Structured Review

Millipore bupropion
Estimation of hydroxybupropion generation by the Huh7-2B6V5 cell line. Huh7-2B6V5 cells were plated on 24-well plates at 80% confluency and then two-days later, media (10% FBS/PS/DMEM) containing 100 mM of <t>bupropion</t> was added for various incubation times. After incubation of substrate, 3 volumes of ACN were added and the plate was frozen and thawed. Cells were broken by pipetting and after spinning down the cell-media mixtures, supernatants were collected to vials for the HRMS analysis (Orbitrap ID-X Tribrid MS). A. Standard curve of S,S-hydroxy and R,R-hydroxy bupropion. B. Quantitation of hydroxy bupropion generation using the R,R-hydroxy bupropion standard. Values are the means ± SD of three individual wells from the same cell preparation. C. Detection of bupropion, hydroxy and di-hydroxy bupropion signals at indicated times from the same experiment as in panel B.
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Images

1) Product Images from "High-throughput Production of Diverse Xenobiotic Metabolites with P450-transduced Huh7 Hepatoma Cell Lines"

Article Title: High-throughput Production of Diverse Xenobiotic Metabolites with P450-transduced Huh7 Hepatoma Cell Lines

Journal: bioRxiv

doi: 10.1101/2022.03.12.484071

Estimation of hydroxybupropion generation by the Huh7-2B6V5 cell line. Huh7-2B6V5 cells were plated on 24-well plates at 80% confluency and then two-days later, media (10% FBS/PS/DMEM) containing 100 mM of bupropion was added for various incubation times. After incubation of substrate, 3 volumes of ACN were added and the plate was frozen and thawed. Cells were broken by pipetting and after spinning down the cell-media mixtures, supernatants were collected to vials for the HRMS analysis (Orbitrap ID-X Tribrid MS). A. Standard curve of S,S-hydroxy and R,R-hydroxy bupropion. B. Quantitation of hydroxy bupropion generation using the R,R-hydroxy bupropion standard. Values are the means ± SD of three individual wells from the same cell preparation. C. Detection of bupropion, hydroxy and di-hydroxy bupropion signals at indicated times from the same experiment as in panel B.
Figure Legend Snippet: Estimation of hydroxybupropion generation by the Huh7-2B6V5 cell line. Huh7-2B6V5 cells were plated on 24-well plates at 80% confluency and then two-days later, media (10% FBS/PS/DMEM) containing 100 mM of bupropion was added for various incubation times. After incubation of substrate, 3 volumes of ACN were added and the plate was frozen and thawed. Cells were broken by pipetting and after spinning down the cell-media mixtures, supernatants were collected to vials for the HRMS analysis (Orbitrap ID-X Tribrid MS). A. Standard curve of S,S-hydroxy and R,R-hydroxy bupropion. B. Quantitation of hydroxy bupropion generation using the R,R-hydroxy bupropion standard. Values are the means ± SD of three individual wells from the same cell preparation. C. Detection of bupropion, hydroxy and di-hydroxy bupropion signals at indicated times from the same experiment as in panel B.

Techniques Used: Incubation, Quantitation Assay

Cell line and substrate specificity. A mixture of 7 substrates at 20 μM final concentration were incubated with each P450-expressing cell line for the indicated times and then quenched with 3 volumes of acetonitrile (ACN) and then analyzed by LC-HRMS (Q Exactive HF mass spectrometer) Only detected signals were plotted. The predicted product masses was selected by 3 criteria: 1) mass ( m/z ) tolerance should be within 0.0005, 2) masses should have the same retention time, and 3) the signal should increase over time. All signals were detected in HILIC positive mode except chlorzoxazone in panel G where the signal was detected in C18 negative mode. A, ethoxyresorufin deethylation (BROD) by CYP1A2 cell line; B, coumarin hydroxylation by CYP2A6 cell line; C, bupropion hydroxylation by CYP2B6 cell line; D, amodiaquine deethylation by CYP2C8; E, omeprazole hydroxylation by CYP2C19 and 3A4 cell lines; F, dextromethorphan demethylation by CYP2D6; G, chlorzoxazone (CLZ) hydroxylation by CYP2E1 (C18). CYP2E1 cell lines were incubated with only chlorzoxazone for the indicated time and analyzed on the same LC-HRMS since we were not able to detect the OH-CLZ from the mixed substrate samples. Values are means ± SD of three individual wells from the same cell preparation.
Figure Legend Snippet: Cell line and substrate specificity. A mixture of 7 substrates at 20 μM final concentration were incubated with each P450-expressing cell line for the indicated times and then quenched with 3 volumes of acetonitrile (ACN) and then analyzed by LC-HRMS (Q Exactive HF mass spectrometer) Only detected signals were plotted. The predicted product masses was selected by 3 criteria: 1) mass ( m/z ) tolerance should be within 0.0005, 2) masses should have the same retention time, and 3) the signal should increase over time. All signals were detected in HILIC positive mode except chlorzoxazone in panel G where the signal was detected in C18 negative mode. A, ethoxyresorufin deethylation (BROD) by CYP1A2 cell line; B, coumarin hydroxylation by CYP2A6 cell line; C, bupropion hydroxylation by CYP2B6 cell line; D, amodiaquine deethylation by CYP2C8; E, omeprazole hydroxylation by CYP2C19 and 3A4 cell lines; F, dextromethorphan demethylation by CYP2D6; G, chlorzoxazone (CLZ) hydroxylation by CYP2E1 (C18). CYP2E1 cell lines were incubated with only chlorzoxazone for the indicated time and analyzed on the same LC-HRMS since we were not able to detect the OH-CLZ from the mixed substrate samples. Values are means ± SD of three individual wells from the same cell preparation.

Techniques Used: Concentration Assay, Incubation, Expressing, Mass Spectrometry, Hydrophilic Interaction Liquid Chromatography

Pharmacokinetics of bupropion and its metabolites, hydroxy and dihydroxybupropion from C57BL mouse after bupropion oral gavage. A. The data for bupropion was published previously ( Mimche et al., 2019 ), and the feature tables were re-analyzed to identify hydroxy and dihydroxybupropion based on their retention times, m/z values and MS 2 spectra. Values are means ± SD of 5 mice in each group. B. Mass fragmentation spectra of 272.1048 m/z (dihydroxybupropion) in 2B6 cell line (red) and in human sample (blue) with documented bupropion use
Figure Legend Snippet: Pharmacokinetics of bupropion and its metabolites, hydroxy and dihydroxybupropion from C57BL mouse after bupropion oral gavage. A. The data for bupropion was published previously ( Mimche et al., 2019 ), and the feature tables were re-analyzed to identify hydroxy and dihydroxybupropion based on their retention times, m/z values and MS 2 spectra. Values are means ± SD of 5 mice in each group. B. Mass fragmentation spectra of 272.1048 m/z (dihydroxybupropion) in 2B6 cell line (red) and in human sample (blue) with documented bupropion use

Techniques Used: Mouse Assay

2) Product Images from "Cytochrome P450 and P-gp Mediated Herb-Drug Interactions and Molecular Docking Studies of Garcinol"

Article Title: Cytochrome P450 and P-gp Mediated Herb-Drug Interactions and Molecular Docking Studies of Garcinol

Journal: Membranes

doi: 10.3390/membranes11120992

Mean plasma concentrations of bupropion ( A ) and midazolam ( B ) after oral administration of garcinol at a dose of 25 mg/kg in rats.
Figure Legend Snippet: Mean plasma concentrations of bupropion ( A ) and midazolam ( B ) after oral administration of garcinol at a dose of 25 mg/kg in rats.

Techniques Used:

IC 50 curves of garcinol for CYP450 activities using the cocktail substrate including CYP1A2 for tacrine 1-hydroxylase, CYP2B6 for bupropion hydroxylase, CYP2C8 for paclitaxel 6-hydroxylase, CYP2C9 for diclofenac 4-hydroxylase, CYP2C19 for S-mephenytoin 4-hydroxylase, CYP2D6 for dextromethorphan O-demethylase, CYP2E1 for chlorzoxazone 6-hydroxylase and CYP3A4 for midazolam 1′-hydroxylase.
Figure Legend Snippet: IC 50 curves of garcinol for CYP450 activities using the cocktail substrate including CYP1A2 for tacrine 1-hydroxylase, CYP2B6 for bupropion hydroxylase, CYP2C8 for paclitaxel 6-hydroxylase, CYP2C9 for diclofenac 4-hydroxylase, CYP2C19 for S-mephenytoin 4-hydroxylase, CYP2D6 for dextromethorphan O-demethylase, CYP2E1 for chlorzoxazone 6-hydroxylase and CYP3A4 for midazolam 1′-hydroxylase.

Techniques Used:

3) Product Images from "Large scale enzyme based xenobiotic identification for exposomics"

Article Title: Large scale enzyme based xenobiotic identification for exposomics

Journal: Nature Communications

doi: 10.1038/s41467-021-25698-x

Identification of documented xenobiotic exposures. Extracted ion chromatograms of blood pharmacokinetic data from mice (black) that received bupropion show a – c bupropion, hydroxybupropion, and hydrobupropion are detected at the same accurate mass m / z and retention time as S9-enzyme generated metabolites (red). These metabolites were not detected in a control sample (blue). Extracted ion chromatograms of plasma collected from an individual (black) taking bupropion shows d – f bupropion, hydroxybupropion, and hydrobupropion are detected at the same accurate mass m/z and retention time as enzyme-generated metabolites (red). g Co-occurrence of bupropion with its expected metabolites only in the samples with documented bupropion use. Relative abundance values were colored across each row using the maximum observed peak intensities (red) and minimum observed peak intensities (blue) for a particular metabolite. h – k Pathway-level biotransformation networking of parent xenobiotics shows expected metabolites with characteristic mass shifts (above red edge) are correlated (Partial least squares regression R value shown below red edge) with parent xenobiotic.
Figure Legend Snippet: Identification of documented xenobiotic exposures. Extracted ion chromatograms of blood pharmacokinetic data from mice (black) that received bupropion show a – c bupropion, hydroxybupropion, and hydrobupropion are detected at the same accurate mass m / z and retention time as S9-enzyme generated metabolites (red). These metabolites were not detected in a control sample (blue). Extracted ion chromatograms of plasma collected from an individual (black) taking bupropion shows d – f bupropion, hydroxybupropion, and hydrobupropion are detected at the same accurate mass m/z and retention time as enzyme-generated metabolites (red). g Co-occurrence of bupropion with its expected metabolites only in the samples with documented bupropion use. Relative abundance values were colored across each row using the maximum observed peak intensities (red) and minimum observed peak intensities (blue) for a particular metabolite. h – k Pathway-level biotransformation networking of parent xenobiotics shows expected metabolites with characteristic mass shifts (above red edge) are correlated (Partial least squares regression R value shown below red edge) with parent xenobiotic.

Techniques Used: Mouse Assay, Generated

Stable-isotope assisted metabolite identification. Use of d 9 -bupropion with S9 enzyme system produces either a d 8 -(2S,3S)-hydroxybupropion or b d 9 -4′-hydroxybupropion. c Extracted ion chromatogram of 264.1600 m / z (d 8 -(2S,3S)-hydroxybupropion) at 0 and 24 h with the addition of d 9 -bupropion. d Extraction ion chromatogram of 265.1674 m / z (d 9 -4′ hydroxybupropion) at 0 and 24 h with addition of d 9 bupropion. e Extracted ion chromatogram of 256.1099 m / z (hydroxybupropion) at 0 and 24 h with addition of bupropion. f Mass fragmentation spectrum (MS 2 ) of 256.1099 m / z (black) is consistent with (2S,3S)-hydroxybupropion.
Figure Legend Snippet: Stable-isotope assisted metabolite identification. Use of d 9 -bupropion with S9 enzyme system produces either a d 8 -(2S,3S)-hydroxybupropion or b d 9 -4′-hydroxybupropion. c Extracted ion chromatogram of 264.1600 m / z (d 8 -(2S,3S)-hydroxybupropion) at 0 and 24 h with the addition of d 9 -bupropion. d Extraction ion chromatogram of 265.1674 m / z (d 9 -4′ hydroxybupropion) at 0 and 24 h with addition of d 9 bupropion. e Extracted ion chromatogram of 256.1099 m / z (hydroxybupropion) at 0 and 24 h with addition of bupropion. f Mass fragmentation spectrum (MS 2 ) of 256.1099 m / z (black) is consistent with (2S,3S)-hydroxybupropion.

Techniques Used:

4) Product Images from "Synthesis and Evaluation of the Antidepressant-like Properties of HBK-10, a Novel 2-Methoxyphenylpiperazine Derivative Targeting the 5-HT1A and D2 Receptors"

Article Title: Synthesis and Evaluation of the Antidepressant-like Properties of HBK-10, a Novel 2-Methoxyphenylpiperazine Derivative Targeting the 5-HT1A and D2 Receptors

Journal: Pharmaceuticals

doi: 10.3390/ph14080744

The effect of fluoxetine (Panel ( A )), reboxetine (Panel ( B )), and bupropion (Panel ( C )) on antidepressant-like activity of HBK-10 in the forced swim test in mice. Studied compound and reference drugs: fluoxetine, reboxetine, and bupropion, were administered ip at sub-effective doses 30 min before the test. The results are presented as box plots showing the following data: mean (‘+’), median (horizontal line), upper and lower quartile (the width of the box shows interquartile range), upper and lower extreme (whiskers). Statistical analysis: Shapiro–Wilk test for normality, Brown–Forsythe test for homogeneity of variance, and two-way ANOVA (Newman–Keuls post hoc); ** p
Figure Legend Snippet: The effect of fluoxetine (Panel ( A )), reboxetine (Panel ( B )), and bupropion (Panel ( C )) on antidepressant-like activity of HBK-10 in the forced swim test in mice. Studied compound and reference drugs: fluoxetine, reboxetine, and bupropion, were administered ip at sub-effective doses 30 min before the test. The results are presented as box plots showing the following data: mean (‘+’), median (horizontal line), upper and lower quartile (the width of the box shows interquartile range), upper and lower extreme (whiskers). Statistical analysis: Shapiro–Wilk test for normality, Brown–Forsythe test for homogeneity of variance, and two-way ANOVA (Newman–Keuls post hoc); ** p

Techniques Used: Activity Assay, Mouse Assay

5) Product Images from "NNAL, a major metabolite of tobacco-specific carcinogen NNK, promotes lung cancer progression through deactivating LKB1 in an isomer-dependent manner"

Article Title: NNAL, a major metabolite of tobacco-specific carcinogen NNK, promotes lung cancer progression through deactivating LKB1 in an isomer-dependent manner

Journal: bioRxiv

doi: 10.1101/2021.06.15.448557

The potential upstream signaling events governing NNAL-promoted phenotypes with pharmacological inhibitors. A. Effect of (R)-NNAL on PKA-Cα nucleus translocation in H1299. Cells were treated with 100 nM (R)-NNAL for 60 min. DAPI was used to stain the nucleus. B. Effect of inhibition of β-ARs (propranolol), Ca 2+ channels (nifedipine), PKA (H89) and α-ARs (yohimbine) on NNAL-promoted cell proliferation and LKB1 phosphorylation (Ser428). H1299 cells were co-treated with 10 nM (R)-NNAL and 0.1 μM nifedipine, 0.1 μM propranolol, 2.5 μM bupropion, 0.5 μM H89 or 0.1 μM yohimbine for 6 days. C. Effect of inhibition of β-ARs (propranolol), Ca 2+ channels (nifedipine), PKA (H89) an α-ARs (yohimbine) on NNAL-promoted resistance to gemcitabine and cisplatin. H1299 cells were co-treated with 40 μM gemcitabine or 120 μM cisplatin along inhibitors. *, P
Figure Legend Snippet: The potential upstream signaling events governing NNAL-promoted phenotypes with pharmacological inhibitors. A. Effect of (R)-NNAL on PKA-Cα nucleus translocation in H1299. Cells were treated with 100 nM (R)-NNAL for 60 min. DAPI was used to stain the nucleus. B. Effect of inhibition of β-ARs (propranolol), Ca 2+ channels (nifedipine), PKA (H89) and α-ARs (yohimbine) on NNAL-promoted cell proliferation and LKB1 phosphorylation (Ser428). H1299 cells were co-treated with 10 nM (R)-NNAL and 0.1 μM nifedipine, 0.1 μM propranolol, 2.5 μM bupropion, 0.5 μM H89 or 0.1 μM yohimbine for 6 days. C. Effect of inhibition of β-ARs (propranolol), Ca 2+ channels (nifedipine), PKA (H89) an α-ARs (yohimbine) on NNAL-promoted resistance to gemcitabine and cisplatin. H1299 cells were co-treated with 40 μM gemcitabine or 120 μM cisplatin along inhibitors. *, P

Techniques Used: Translocation Assay, Staining, Inhibition

6) Product Images from "Disruption of the cholinergic anti-inflammatory response by R5-tropic HIV-1 protein gp120JRFL"

Article Title: Disruption of the cholinergic anti-inflammatory response by R5-tropic HIV-1 protein gp120JRFL

Journal: The Journal of Biological Chemistry

doi: 10.1016/j.jbc.2021.100618

Bupropion limitedly restores the CAR in MDMs. α7-nAChR partial antagonist bupropion significantly decreased the levels of IL-6 but not the remaining cytokines in α7-nAChR upregulated MDMs. IL-10 levels remained unaltered. Results were normalized to LPS-induced cytokine release. Incubation time for gp120 JRFL was 72 h. Normalized response equals the cytokine concentration in α7-nAChR upregulated MDMs in the presence of bupropion, LPS plus ACh, and divided by the concentration reached with LPS alone (Bup.+LPS+ACh/LPS). Statistical analysis was carried out using One-sample t -test; n = 5 to 7 subjects; ∗ p ≤ 0.05, all values were normalized.
Figure Legend Snippet: Bupropion limitedly restores the CAR in MDMs. α7-nAChR partial antagonist bupropion significantly decreased the levels of IL-6 but not the remaining cytokines in α7-nAChR upregulated MDMs. IL-10 levels remained unaltered. Results were normalized to LPS-induced cytokine release. Incubation time for gp120 JRFL was 72 h. Normalized response equals the cytokine concentration in α7-nAChR upregulated MDMs in the presence of bupropion, LPS plus ACh, and divided by the concentration reached with LPS alone (Bup.+LPS+ACh/LPS). Statistical analysis was carried out using One-sample t -test; n = 5 to 7 subjects; ∗ p ≤ 0.05, all values were normalized.

Techniques Used: Incubation, Concentration Assay

7) Product Images from "Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver Microsomes"

Article Title: Strong and Selective Inhibitory Effects of the Biflavonoid Selamariscina A against CYP2C8 and CYP2C9 Enzyme Activities in Human Liver Microsomes

Journal: Pharmaceutics

doi: 10.3390/pharmaceutics12040343

Representative Dixon plots obtained from a kinetic study of CYP1A2-catalyzed phenacetin O -deethylation ( A ), CYP2B6-catalyzed bupropion hydroxylation ( B ), CYP2C8-catalyzed amodiaquine N-deethylation ( C ), CYP2C8-catalyzed rosiglitazone 5-hydroxylation ( D ), CYP2C9-catalyzed diclofenac 4-hydroxylation ( E ), and CYP3A-catalyzed midazolam 1′-hydroxylation ( F ) in the presence of different concentrations of selamariscina A in pooled human liver microsomes (XTreme 200, XenoTech). Each data point shown represent the mean ± standard error in triplicate for the samples.
Figure Legend Snippet: Representative Dixon plots obtained from a kinetic study of CYP1A2-catalyzed phenacetin O -deethylation ( A ), CYP2B6-catalyzed bupropion hydroxylation ( B ), CYP2C8-catalyzed amodiaquine N-deethylation ( C ), CYP2C8-catalyzed rosiglitazone 5-hydroxylation ( D ), CYP2C9-catalyzed diclofenac 4-hydroxylation ( E ), and CYP3A-catalyzed midazolam 1′-hydroxylation ( F ) in the presence of different concentrations of selamariscina A in pooled human liver microsomes (XTreme 200, XenoTech). Each data point shown represent the mean ± standard error in triplicate for the samples.

Techniques Used:

Inhibitory effects of selamariscina A (0.5 μM, ☐) and montelukast (0.5 μM, ■; 5 μM, ■ ) on the enzymatic activities of nine P450 isoforms in pooled human liver microsomes (0.25 mg/mL, XTreme 200, XenoTech). Phenacetin (100 μM), coumarin (5 μM), bupropion (50 μM), amodiaquine (1 μM), diclofenac (10 μM), omeprazole (20 μM), dextromethorphan (5 μM), chlorzoxazone (50 μM), and midazolam (5 μM) were used as the respective substrates of P450s 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, and 3A. The data are means of the average ± standard error in triplicate.
Figure Legend Snippet: Inhibitory effects of selamariscina A (0.5 μM, ☐) and montelukast (0.5 μM, ■; 5 μM, ■ ) on the enzymatic activities of nine P450 isoforms in pooled human liver microsomes (0.25 mg/mL, XTreme 200, XenoTech). Phenacetin (100 μM), coumarin (5 μM), bupropion (50 μM), amodiaquine (1 μM), diclofenac (10 μM), omeprazole (20 μM), dextromethorphan (5 μM), chlorzoxazone (50 μM), and midazolam (5 μM) were used as the respective substrates of P450s 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, and 3A. The data are means of the average ± standard error in triplicate.

Techniques Used:

8) Product Images from "Development and Application of TK6-derived Cells Expressing Human Cytochrome P450s for Genotoxicity Testing"

Article Title: Development and Application of TK6-derived Cells Expressing Human Cytochrome P450s for Genotoxicity Testing

Journal: Toxicological Sciences

doi: 10.1093/toxsci/kfaa035

A, Characterization of CYP protein expression in stably transduced TK6 cells. The protein levels of CYP isoforms ranging in molecular weight between 45 and 60 kDa were detected by Western blotting. Myc was used as a tag for transfection and GAPDH (37 kDa) was used as a loading control. Similar results were obtained from 3 independent experiments. B, Chromatograms of LC-MS showing the enzymatic activities in the TK6 cells transduced with various CYPs. Abbreviations: APAP, acetaminophen; 7-HFC, 7-hydroxy-4-(trifluoromethyl) coumarin; 7-HC, 7-hydroxycoumarin; HB, hydroxy bupropion; 4-HD, 4-hydroxydiclofenac; 5-HO, 5-hydroxyomeprazole; 1-HM, 1-hydroxymidazolam.
Figure Legend Snippet: A, Characterization of CYP protein expression in stably transduced TK6 cells. The protein levels of CYP isoforms ranging in molecular weight between 45 and 60 kDa were detected by Western blotting. Myc was used as a tag for transfection and GAPDH (37 kDa) was used as a loading control. Similar results were obtained from 3 independent experiments. B, Chromatograms of LC-MS showing the enzymatic activities in the TK6 cells transduced with various CYPs. Abbreviations: APAP, acetaminophen; 7-HFC, 7-hydroxy-4-(trifluoromethyl) coumarin; 7-HC, 7-hydroxycoumarin; HB, hydroxy bupropion; 4-HD, 4-hydroxydiclofenac; 5-HO, 5-hydroxyomeprazole; 1-HM, 1-hydroxymidazolam.

Techniques Used: Expressing, Stable Transfection, Molecular Weight, Western Blot, Transfection, Liquid Chromatography with Mass Spectroscopy, Transduction

9) Product Images from "Pharmacogenomics of poor drug metabolism in Greyhounds: Cytochrome P450 (CYP) 2B11 genetic variation, breed distribution, and functional characterization"

Article Title: Pharmacogenomics of poor drug metabolism in Greyhounds: Cytochrome P450 (CYP) 2B11 genetic variation, breed distribution, and functional characterization

Journal: Scientific Reports

doi: 10.1038/s41598-019-56660-z

Reaction phenotyping using a panel of recombinant canine CYP enzymes. The rates of propofol 4-hydroxylation ( a,b ) bupropion 6-hydroxylation ( c,d ) and omeprazole sulfonation ( e,f ) were determined using a panel of 11 recombinant canine CYP enzymes. Results are shown after normalization to incubation time and recombinant CYP concentration in each reaction ( a,c,e ) as well as after extrapolation of activities to microsomes using the reported average molar concentration of each CYP in canine liver microsomes ( b,d,f ). Details are provided in Materials and Methods section. Activities for pooled dog liver microsomes (pDLMs) normalized to microsomal protein content are also shown for comparison. Bars represent the mean and standard deviation of 3 independent replicate experiments.
Figure Legend Snippet: Reaction phenotyping using a panel of recombinant canine CYP enzymes. The rates of propofol 4-hydroxylation ( a,b ) bupropion 6-hydroxylation ( c,d ) and omeprazole sulfonation ( e,f ) were determined using a panel of 11 recombinant canine CYP enzymes. Results are shown after normalization to incubation time and recombinant CYP concentration in each reaction ( a,c,e ) as well as after extrapolation of activities to microsomes using the reported average molar concentration of each CYP in canine liver microsomes ( b,d,f ). Details are provided in Materials and Methods section. Activities for pooled dog liver microsomes (pDLMs) normalized to microsomal protein content are also shown for comparison. Bars represent the mean and standard deviation of 3 independent replicate experiments.

Techniques Used: Recombinant, Incubation, Concentration Assay, Standard Deviation

10) Product Images from "Inhibition of cytochrome P450 2B6 by Astragalus extract mixture HT042"

Article Title: Inhibition of cytochrome P450 2B6 by Astragalus extract mixture HT042

Journal: Toxicological Research

doi: 10.1007/s43188-019-00027-z

UPLC–MS/MS analysis of bupropion hydroxylation by P450 2B6. Chromatograms of hydroxybupropion and bupropion in the multiple reaction mode (MRM). The positive ionization transitions of bupropion (m/z 240 > 184) and hydroxybupropion (m/z 256.1 > 238.1) were monitored
Figure Legend Snippet: UPLC–MS/MS analysis of bupropion hydroxylation by P450 2B6. Chromatograms of hydroxybupropion and bupropion in the multiple reaction mode (MRM). The positive ionization transitions of bupropion (m/z 240 > 184) and hydroxybupropion (m/z 256.1 > 238.1) were monitored

Techniques Used: Tandem Mass Spectroscopy

11) Product Images from "The Response of Ventral Tegmental Area Dopaminergic Neurons to Bupropion: Excitation or Inhibition?"

Article Title: The Response of Ventral Tegmental Area Dopaminergic Neurons to Bupropion: Excitation or Inhibition?

Journal: Basic and Clinical Neuroscience

doi: 10.32598/bcn.9.10.250

The response of VTA dopaminergic neurons to microiontophoretic application of the bupropion A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery before and after microiontophoretic application of bupropion (-500 nA, 1 mol, pH=4.5, 5 min, at 11 th to 15 th min). The average firing rate of the before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the VTA dopaminergic neuron in each period. The inhibitory periods with the least firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound inhibition in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing of the pre-ejection period was 4.14±0.2 spikes/second. The post-ejection period is included in a period with inhibition of the neuron that began at 11 th to 75 th min of the recording. In the inhibition period, the firing rate decreased to 1.5±1.4 spikes/second with a minimum of 0 spikes/second firing in the 35 th to 52 nd min of recording. The recovery period was the period that the firing rate returned to its pre-injection period (4.3±0.2 spikes/second). The middle histogram shows the comparison of the neuronal firing in the pre-ejection, inhibition, and recovery periods. The mean firing rate of the inhibition period showed a statistically significant difference. One-way repeated measures ANOVA with the Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with the significant levels of *** P
Figure Legend Snippet: The response of VTA dopaminergic neurons to microiontophoretic application of the bupropion A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery before and after microiontophoretic application of bupropion (-500 nA, 1 mol, pH=4.5, 5 min, at 11 th to 15 th min). The average firing rate of the before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the VTA dopaminergic neuron in each period. The inhibitory periods with the least firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound inhibition in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing of the pre-ejection period was 4.14±0.2 spikes/second. The post-ejection period is included in a period with inhibition of the neuron that began at 11 th to 75 th min of the recording. In the inhibition period, the firing rate decreased to 1.5±1.4 spikes/second with a minimum of 0 spikes/second firing in the 35 th to 52 nd min of recording. The recovery period was the period that the firing rate returned to its pre-injection period (4.3±0.2 spikes/second). The middle histogram shows the comparison of the neuronal firing in the pre-ejection, inhibition, and recovery periods. The mean firing rate of the inhibition period showed a statistically significant difference. One-way repeated measures ANOVA with the Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with the significant levels of *** P

Techniques Used: Injection, Isolation, Inhibition

Cumulative data that present the direct inhibition of the Bupropion (BP) on the VTA dopaminergic neurons The effect of Microiontophoretic (MI) and Intracerebroventricular (ICV) application of the bupropion on the percentage of inhibited neurons, percentage of excited neurons, inhibition duration, excitation duration, and silent duration of the VTA dopaminergic neurons in different groups. Bupropion inhibited 97.5%, 70.1%, and 30.4% of VTA dopaminergic neurons at -500, -300, -150 nA, respectively without response at -50 nA. The percentages of inhibited neurons in ICV application of bupropion were 56%, 43%, 33%, 20%, 12%, and 3% at amounts of 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, respectively. The percentage of excited neurons in MI application of bupropion was 0% but they were 42%, 29%, 18%, 11%, 5%, and 2 % at 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol in ICV application of bupropion, respectively. The Mean±SD duration periods of inhibition were 70±13, 45±11, 23±7 min at -500, -300, -150 nA, respectively without any inhibition at -50 nA. The Mean±SD duration periods of inhibition of neurons in the ICV application of bupropion were 56±11, 48±8, 24±4, 10±3, 5±1 min at the amounts of 1, 0.5, 0.1, 0.01, 0.001 mol, respectively without inhibition at 0.0001 mol. The mean excitation duration in MI application of bupropion was 0, but in the ICV application of bupropion, they were 32±10, 21±5, 11±4, 7±3, 2±2 min at amounts of 1, 0.5, 0.1, 0.01, 0.001 mol, respectively without excitation at 0.0001 mol. The MI application of bupropion made VTA dopaminergic neurons silent for 18±8, 12±4, 6±3 min at -500, -300, -150 nA, respectively without any silent neurons at -50 nA. The ICV application of bupropion made VTA dopaminergic neurons silent for 5±2, and 2±2 at 1 and 0.5 mol, respectively. However, there were no silent neurons at the remaining amounts. The crosstab statistical test was used for statistical evaluation of descriptive data (percentage of inhibited and excited neurons). One-way repeated measures ANOVA and Tukey’s post hoc test were used for quantitating data evaluation. The data are presented as Mean±SD with significant levels of *** P
Figure Legend Snippet: Cumulative data that present the direct inhibition of the Bupropion (BP) on the VTA dopaminergic neurons The effect of Microiontophoretic (MI) and Intracerebroventricular (ICV) application of the bupropion on the percentage of inhibited neurons, percentage of excited neurons, inhibition duration, excitation duration, and silent duration of the VTA dopaminergic neurons in different groups. Bupropion inhibited 97.5%, 70.1%, and 30.4% of VTA dopaminergic neurons at -500, -300, -150 nA, respectively without response at -50 nA. The percentages of inhibited neurons in ICV application of bupropion were 56%, 43%, 33%, 20%, 12%, and 3% at amounts of 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, respectively. The percentage of excited neurons in MI application of bupropion was 0% but they were 42%, 29%, 18%, 11%, 5%, and 2 % at 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol in ICV application of bupropion, respectively. The Mean±SD duration periods of inhibition were 70±13, 45±11, 23±7 min at -500, -300, -150 nA, respectively without any inhibition at -50 nA. The Mean±SD duration periods of inhibition of neurons in the ICV application of bupropion were 56±11, 48±8, 24±4, 10±3, 5±1 min at the amounts of 1, 0.5, 0.1, 0.01, 0.001 mol, respectively without inhibition at 0.0001 mol. The mean excitation duration in MI application of bupropion was 0, but in the ICV application of bupropion, they were 32±10, 21±5, 11±4, 7±3, 2±2 min at amounts of 1, 0.5, 0.1, 0.01, 0.001 mol, respectively without excitation at 0.0001 mol. The MI application of bupropion made VTA dopaminergic neurons silent for 18±8, 12±4, 6±3 min at -500, -300, -150 nA, respectively without any silent neurons at -50 nA. The ICV application of bupropion made VTA dopaminergic neurons silent for 5±2, and 2±2 at 1 and 0.5 mol, respectively. However, there were no silent neurons at the remaining amounts. The crosstab statistical test was used for statistical evaluation of descriptive data (percentage of inhibited and excited neurons). One-way repeated measures ANOVA and Tukey’s post hoc test were used for quantitating data evaluation. The data are presented as Mean±SD with significant levels of *** P

Techniques Used: Inhibition

The figure of the VTA dopaminergic neurons to intracerebroventricular application of the bupropion with excitatory effects A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery after microinjection of bupropion (1 mol, 5 μL/3min, at 11 th to 13 th min) into the ipsilateral ventricle. The average firing rate before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the isolated VTA dopaminergic neuron in each period. The excitatory periods with the highest firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound excitation in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing rate of the pre-injection period was 4.8±0.24 spikes/second. The post-injection period was included in a period with excitation of the neuron, that began at 12 th to 68 th min of the recording. In the excitation period, the firing rate increased to 7.01±1.96 spikes/second with a maximum of firing 10.8 spikes/second in the 33 rd min. The recovery period was determined by firing that came back to its pre-injection value.The mean firing rate of the excitation period showed a statistically significant difference. One-Way repeated measures Analysis of Variance (ANOVA) with the Tukey’s post hoc test were used for statistical evaluation. The data are represented as Mean±SD with a significant level of *** P
Figure Legend Snippet: The figure of the VTA dopaminergic neurons to intracerebroventricular application of the bupropion with excitatory effects A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery after microinjection of bupropion (1 mol, 5 μL/3min, at 11 th to 13 th min) into the ipsilateral ventricle. The average firing rate before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the isolated VTA dopaminergic neuron in each period. The excitatory periods with the highest firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound excitation in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing rate of the pre-injection period was 4.8±0.24 spikes/second. The post-injection period was included in a period with excitation of the neuron, that began at 12 th to 68 th min of the recording. In the excitation period, the firing rate increased to 7.01±1.96 spikes/second with a maximum of firing 10.8 spikes/second in the 33 rd min. The recovery period was determined by firing that came back to its pre-injection value.The mean firing rate of the excitation period showed a statistically significant difference. One-Way repeated measures Analysis of Variance (ANOVA) with the Tukey’s post hoc test were used for statistical evaluation. The data are represented as Mean±SD with a significant level of *** P

Techniques Used: Injection, Isolation

The firing of the VTA dopaminergic neurons in the sham group with the intracerebroventricular application of the bupropion A. The firing of sample VTA dopaminergic multiunit neurons in the sham group. In the sham group, the VTA dopaminergic neuronal firings under standard condition were recorded up to 120 min. Bupropion vehicle (sterile ACSF, 5 μL/3min, in 11 th to 13 th min) was injected by 30-gauge Hamilton syringe in the core of right ventricle with motorized programmable pump; B. The histogram of the neuronal firing rate in the recorded neurons. The Mean±SD neuronal firing rate was 5.34±0.5 spikes/second. Vehicle had no significant effect on the neuronal firing. The paired student t-test was used for statistical analysis. The data are presented as Mean±SD.
Figure Legend Snippet: The firing of the VTA dopaminergic neurons in the sham group with the intracerebroventricular application of the bupropion A. The firing of sample VTA dopaminergic multiunit neurons in the sham group. In the sham group, the VTA dopaminergic neuronal firings under standard condition were recorded up to 120 min. Bupropion vehicle (sterile ACSF, 5 μL/3min, in 11 th to 13 th min) was injected by 30-gauge Hamilton syringe in the core of right ventricle with motorized programmable pump; B. The histogram of the neuronal firing rate in the recorded neurons. The Mean±SD neuronal firing rate was 5.34±0.5 spikes/second. Vehicle had no significant effect on the neuronal firing. The paired student t-test was used for statistical analysis. The data are presented as Mean±SD.

Techniques Used: Injection

The response of the VTA dopaminergic neurons to intracerebroventricular application of the bupropion with inhibitory effects. A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery before and after microinjection of bupropion (1 mol, 5 μL/3min, at 11 th to 13 th min) into the ipsilateral ventricle. The average firing rates of the before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the VTA dopaminergic neuron in each period. The inhibitory periods with the least firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound inhibition in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing rate of the pre-injection period was 6.3±0.14 spikes/second. The post-injection period was included in a period with inhibition of the neuron that began at 14th to 68th min of the recording. In the inhibition period, the, Mean±SD firing rate decreased to 3±1.94 spikes/second with a minimum of 0 spikes/second firing in the 44 th to 48 th min of recording. The recovery period was the period that the firing rate returned to its pre-injection period (6.27±0.19 spikes/second). The middle bar graph shows the comparison of the neuronal firing in the pre-injection, inhibition, and recovery periods. The mean firing rate of the inhibition period showed a statistically significant difference. One-way repeated measures ANOVA with the Tukey’s post hoc test were used for statistical evaluation. The data are presented as Mean±SD with significant level of *** P
Figure Legend Snippet: The response of the VTA dopaminergic neurons to intracerebroventricular application of the bupropion with inhibitory effects. A. A sample of the multiunit recording shows the recorded trace in three phases of pre-injection, post-injection, and recovery before and after microinjection of bupropion (1 mol, 5 μL/3min, at 11 th to 13 th min) into the ipsilateral ventricle. The average firing rates of the before and after consecutive minutes for each minute was calculated for determining the statistical difference for each minute of the isolated unit; B. The bar graph of the average firing rate of the VTA dopaminergic neuron in each period. The inhibitory periods with the least firing rate has a statistical difference with pre-injection and recovery periods. Bupropion elicited a profound inhibition in the neuron; C. Continuous histogram of mean firing rate in three mentioned phases. The Mean±SD firing rate of the pre-injection period was 6.3±0.14 spikes/second. The post-injection period was included in a period with inhibition of the neuron that began at 14th to 68th min of the recording. In the inhibition period, the, Mean±SD firing rate decreased to 3±1.94 spikes/second with a minimum of 0 spikes/second firing in the 44 th to 48 th min of recording. The recovery period was the period that the firing rate returned to its pre-injection period (6.27±0.19 spikes/second). The middle bar graph shows the comparison of the neuronal firing in the pre-injection, inhibition, and recovery periods. The mean firing rate of the inhibition period showed a statistically significant difference. One-way repeated measures ANOVA with the Tukey’s post hoc test were used for statistical evaluation. The data are presented as Mean±SD with significant level of *** P

Techniques Used: Injection, Isolation, Inhibition

Bar graph of the inhibition effect of bupropion on the VTA-DA neurons in different groups A. The graph shows the mean firing rate of the ventral tegmental area dopaminergic neurons to different amount of bupropion application (intracerebroventricular, 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, 5 μL/3min, at 11 th to 13 th min) and lower graph; B. Shows the percentages of firing rate according to the pre-injection firing as 100%. Bupropion inhibited the neurons dose-dependently. There were significant differences in the mean firing rate of the inhibition period of 1, 0.5, 0.1, and 0.01 mol of bupropion but the amounts of 0.001 and 0.0001 mol did not show any significant difference. One-way repeated measures ANOVA with Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with significant level of *** P
Figure Legend Snippet: Bar graph of the inhibition effect of bupropion on the VTA-DA neurons in different groups A. The graph shows the mean firing rate of the ventral tegmental area dopaminergic neurons to different amount of bupropion application (intracerebroventricular, 1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, 5 μL/3min, at 11 th to 13 th min) and lower graph; B. Shows the percentages of firing rate according to the pre-injection firing as 100%. Bupropion inhibited the neurons dose-dependently. There were significant differences in the mean firing rate of the inhibition period of 1, 0.5, 0.1, and 0.01 mol of bupropion but the amounts of 0.001 and 0.0001 mol did not show any significant difference. One-way repeated measures ANOVA with Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with significant level of *** P

Techniques Used: Inhibition, Injection

Bar graph of the excitation response of the VTA dopaminergic neurons to the intracerebroventricular application of bupropion in different groups The upper graph shows the mean of firing rate of the VTA dopaminergic neurons per different amount of bupropion (1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, 5 μl/3min, at 11 th to 13 th min) and the lower graph shows the percentage of firing rate according to the pre-injection firing as 100%. Bupropion could excite the neurons dose-dependently. There were significant differences between the mean firing rates of the excitation periods of 1, 0.5, 0.1, and 0.01 mol of bupropion but the amounts of 0.001 and 0.0001 mol did not show any significant difference. One-way repeated measures ANOVA with Tukey’s post hoc test were used for statistical evaluation. The data are represented as Man±SD with significant levels of *** P
Figure Legend Snippet: Bar graph of the excitation response of the VTA dopaminergic neurons to the intracerebroventricular application of bupropion in different groups The upper graph shows the mean of firing rate of the VTA dopaminergic neurons per different amount of bupropion (1, 0.5, 0.1, 0.01, 0.001, and 0.0001 mol, 5 μl/3min, at 11 th to 13 th min) and the lower graph shows the percentage of firing rate according to the pre-injection firing as 100%. Bupropion could excite the neurons dose-dependently. There were significant differences between the mean firing rates of the excitation periods of 1, 0.5, 0.1, and 0.01 mol of bupropion but the amounts of 0.001 and 0.0001 mol did not show any significant difference. One-way repeated measures ANOVA with Tukey’s post hoc test were used for statistical evaluation. The data are represented as Man±SD with significant levels of *** P

Techniques Used: Injection

Bar graph of the inhibition of the VTA dopaminergic neurons to microiontophoretic application of the bupropion in different amounts A. The upper graph shows the mean firing rate of the VTA dopaminergic neurons at different amounts of bupropion application (-500, -300, -150, and -50 nA, 1 mol, pH=4.5, at 11 th to 15 th min); B. The lower graph shows the percentage of the firing rate according to the pre-injection firing as 100%. Bupropion inhibited the neurons dose-dependently. There were significant differences between the mean firing rate of the inhibition period of -500, -300, and -150 nA of bupropion but the amount of -50 nA did not show any significant difference. One-way repeated measures ANOVA and the Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with significant levels of *** P
Figure Legend Snippet: Bar graph of the inhibition of the VTA dopaminergic neurons to microiontophoretic application of the bupropion in different amounts A. The upper graph shows the mean firing rate of the VTA dopaminergic neurons at different amounts of bupropion application (-500, -300, -150, and -50 nA, 1 mol, pH=4.5, at 11 th to 15 th min); B. The lower graph shows the percentage of the firing rate according to the pre-injection firing as 100%. Bupropion inhibited the neurons dose-dependently. There were significant differences between the mean firing rate of the inhibition period of -500, -300, and -150 nA of bupropion but the amount of -50 nA did not show any significant difference. One-way repeated measures ANOVA and the Tukey’s Post Hoc test were used for statistical evaluation. The data are represented as Mean±SD with significant levels of *** P

Techniques Used: Inhibition, Injection

12) Product Images from "Neuroprotective Effects of Forced Exercise and Bupropion on Chronic Methamphetamine-induced Cognitive Impairment via Modulation of cAMP Response Element-binding Protein/Brain-derived Neurotrophic Factor Signaling Pathway, Oxidative Stress, and Inflammatory Biomarkers in Rats"

Article Title: Neuroprotective Effects of Forced Exercise and Bupropion on Chronic Methamphetamine-induced Cognitive Impairment via Modulation of cAMP Response Element-binding Protein/Brain-derived Neurotrophic Factor Signaling Pathway, Oxidative Stress, and Inflammatory Biomarkers in Rats

Journal: Advanced Biomedical Research

doi: 10.4103/abr.abr_11_18

Alterations of expression/level (ELISA) of cAMP response element-binding protein (total form) (a), phosphorylated forms of cAMP response element-binding protein, (b) and brain-derived neurotrophic factor (c) in hippocampus in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, P-CREB: Phosphorylated forms of cAMP response element-binding protein. ***Significant level with P
Figure Legend Snippet: Alterations of expression/level (ELISA) of cAMP response element-binding protein (total form) (a), phosphorylated forms of cAMP response element-binding protein, (b) and brain-derived neurotrophic factor (c) in hippocampus in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, P-CREB: Phosphorylated forms of cAMP response element-binding protein. ***Significant level with P

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Binding Assay, Derivative Assay, Negative Control, Positive Control

An average of escape latency (a), traveled distance (b), swimming speed, (c) and percentages of time spent in target quarter in probe trial (d) in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise across all training days by using Morris water maze in rats. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, MWM: Morris water maze. ***Significant level with P
Figure Legend Snippet: An average of escape latency (a), traveled distance (b), swimming speed, (c) and percentages of time spent in target quarter in probe trial (d) in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise across all training days by using Morris water maze in rats. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, MWM: Morris water maze. ***Significant level with P

Techniques Used: Negative Control, Positive Control

13) Product Images from "Neuroprotective Effects of Forced Exercise and Bupropion on Chronic Methamphetamine-induced Cognitive Impairment via Modulation of cAMP Response Element-binding Protein/Brain-derived Neurotrophic Factor Signaling Pathway, Oxidative Stress, and Inflammatory Biomarkers in Rats"

Article Title: Neuroprotective Effects of Forced Exercise and Bupropion on Chronic Methamphetamine-induced Cognitive Impairment via Modulation of cAMP Response Element-binding Protein/Brain-derived Neurotrophic Factor Signaling Pathway, Oxidative Stress, and Inflammatory Biomarkers in Rats

Journal: Advanced Biomedical Research

doi: 10.4103/abr.abr_11_18

Alterations of expression/level (ELISA) of cAMP response element-binding protein (total form) (a), phosphorylated forms of cAMP response element-binding protein, (b) and brain-derived neurotrophic factor (c) in hippocampus in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, P-CREB: Phosphorylated forms of cAMP response element-binding protein. ***Significant level with P
Figure Legend Snippet: Alterations of expression/level (ELISA) of cAMP response element-binding protein (total form) (a), phosphorylated forms of cAMP response element-binding protein, (b) and brain-derived neurotrophic factor (c) in hippocampus in negative control group and group under treatment with 10 mg/kg of methamphetamine (positive control) and groups under treatment by methamphetamine in combination with bupropion (20 mg/kg), forced exercise, or under bupropion in combination with forced exercise. All data are expressed as mean ± standard error of the mean ( n = 8). METH: Methamphetamine, P-CREB: Phosphorylated forms of cAMP response element-binding protein. ***Significant level with P

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Binding Assay, Derivative Assay, Negative Control, Positive Control

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    Millipore bupropion hydrochloride
    Escitalopram- and <t>bupropion-injected</t> mouse behavior in tail suspension test. Behavior in the tail suspension test (TST) was normalized to same-sex and same-genotype saline-injected mice (yellow, 10 mL/kg) to best evaluate how injections of escitalopram (light blue, 1 mg/kg; dark blue, 2 mg/kg) or bupropion (light red, 4 mg/kg; dark red, 8 mg/kg) affected TST behavior in female ( A , B ) and male ( C , D ) PMAT wildtype (+/+, black squares), PMAT heterozygote (+/−, grey diamonds), and PMAT knockout (−/−, open circles) mice. Data were graphed as percent change from the same-sex and same-genotype saline-injected mice for time spent immobile ( A , C ) and latency to the first bout of immobility ( B , D ), based on scoring offline by an observer blinded to treatment and genotype. Data are shown as individual points in violin plots, with horizontal lines indicating median and quartiles. The dashed line across all graphs indicates the mean of 100% for saline-injected controls. * p
    Bupropion Hydrochloride, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bupropion hydrochloride/product/Millipore
    Average 91 stars, based on 1 article reviews
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    bupropion hydrochloride - by Bioz Stars, 2022-11
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    Millipore bupropion
    The effect of fluoxetine (Panel ( A )), reboxetine (Panel ( B )), and <t>bupropion</t> (Panel ( C )) on antidepressant-like activity of HBK-10 in the forced swim test in mice. Studied compound and reference drugs: fluoxetine, reboxetine, and bupropion, were administered ip at sub-effective doses 30 min before the test. The results are presented as box plots showing the following data: mean (‘+’), median (horizontal line), upper and lower quartile (the width of the box shows interquartile range), upper and lower extreme (whiskers). Statistical analysis: Shapiro–Wilk test for normality, Brown–Forsythe test for homogeneity of variance, and two-way ANOVA (Newman–Keuls post hoc); ** p
    Bupropion, supplied by Millipore, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bupropion/product/Millipore
    Average 80 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    Escitalopram- and bupropion-injected mouse behavior in tail suspension test. Behavior in the tail suspension test (TST) was normalized to same-sex and same-genotype saline-injected mice (yellow, 10 mL/kg) to best evaluate how injections of escitalopram (light blue, 1 mg/kg; dark blue, 2 mg/kg) or bupropion (light red, 4 mg/kg; dark red, 8 mg/kg) affected TST behavior in female ( A , B ) and male ( C , D ) PMAT wildtype (+/+, black squares), PMAT heterozygote (+/−, grey diamonds), and PMAT knockout (−/−, open circles) mice. Data were graphed as percent change from the same-sex and same-genotype saline-injected mice for time spent immobile ( A , C ) and latency to the first bout of immobility ( B , D ), based on scoring offline by an observer blinded to treatment and genotype. Data are shown as individual points in violin plots, with horizontal lines indicating median and quartiles. The dashed line across all graphs indicates the mean of 100% for saline-injected controls. * p

    Journal: Cells

    Article Title: Uncovering Functional Contributions of PMAT (Slc29a4) to Monoamine Clearance Using Pharmacobehavioral Tools

    doi: 10.3390/cells11121874

    Figure Lengend Snippet: Escitalopram- and bupropion-injected mouse behavior in tail suspension test. Behavior in the tail suspension test (TST) was normalized to same-sex and same-genotype saline-injected mice (yellow, 10 mL/kg) to best evaluate how injections of escitalopram (light blue, 1 mg/kg; dark blue, 2 mg/kg) or bupropion (light red, 4 mg/kg; dark red, 8 mg/kg) affected TST behavior in female ( A , B ) and male ( C , D ) PMAT wildtype (+/+, black squares), PMAT heterozygote (+/−, grey diamonds), and PMAT knockout (−/−, open circles) mice. Data were graphed as percent change from the same-sex and same-genotype saline-injected mice for time spent immobile ( A , C ) and latency to the first bout of immobility ( B , D ), based on scoring offline by an observer blinded to treatment and genotype. Data are shown as individual points in violin plots, with horizontal lines indicating median and quartiles. The dashed line across all graphs indicates the mean of 100% for saline-injected controls. * p

    Article Snippet: Bupropion hydrochloride (PHR1730), escitalopram oxalate (E4786), cocaine hydrochloride (C5776), and D-amphetamine hemisulfate salt (A5880) were all purchased from Sigma Aldrich (St. Louis, MO, USA).

    Techniques: Injection, Mouse Assay, Knock-Out

    Escitalopram- and bupropion-injected mouse locomotor behavior. Locomotor behavior in the open field was not different across sex nor genotype in saline-injected (yellow, 10 mL/kg) PMAT wildtype (+/+, black squares), PMAT heterozygote (+/−, grey diamonds), and PMAT knockout (−/−, open circles) mice ( A ). Locomotor data were normalized to same-sex and same-genotype saline-injected mice to best evaluate how injections of escitalopram (light blue, 1 mg/kg; dark blue, 2 mg/kg) or bupropion (light red, 4 mg/kg; dark red, 8 mg/kg) affected locomotor behavior in female ( B ) and male ( C ) PMAT mice. Data were graphed as percent change from the same-sex and same-genotype saline-injected mice for distance traveled, as quantified by ANY-maze software. Data are shown as individual points in violin plots, with horizontal lines indicating median and quartiles. The dashed line across ( B , C ) indicates the mean of 100% for saline-injected controls. * p

    Journal: Cells

    Article Title: Uncovering Functional Contributions of PMAT (Slc29a4) to Monoamine Clearance Using Pharmacobehavioral Tools

    doi: 10.3390/cells11121874

    Figure Lengend Snippet: Escitalopram- and bupropion-injected mouse locomotor behavior. Locomotor behavior in the open field was not different across sex nor genotype in saline-injected (yellow, 10 mL/kg) PMAT wildtype (+/+, black squares), PMAT heterozygote (+/−, grey diamonds), and PMAT knockout (−/−, open circles) mice ( A ). Locomotor data were normalized to same-sex and same-genotype saline-injected mice to best evaluate how injections of escitalopram (light blue, 1 mg/kg; dark blue, 2 mg/kg) or bupropion (light red, 4 mg/kg; dark red, 8 mg/kg) affected locomotor behavior in female ( B ) and male ( C ) PMAT mice. Data were graphed as percent change from the same-sex and same-genotype saline-injected mice for distance traveled, as quantified by ANY-maze software. Data are shown as individual points in violin plots, with horizontal lines indicating median and quartiles. The dashed line across ( B , C ) indicates the mean of 100% for saline-injected controls. * p

    Article Snippet: Bupropion hydrochloride (PHR1730), escitalopram oxalate (E4786), cocaine hydrochloride (C5776), and D-amphetamine hemisulfate salt (A5880) were all purchased from Sigma Aldrich (St. Louis, MO, USA).

    Techniques: Injection, Knock-Out, Mouse Assay, Software

    Vagus-dependent antidepressants had a unique spike firing pattern code that was disrupted by inhibition of IPAN to vagus synaptic transmission. ( A ) Diagram of stylised single unit discharge illustrating the 4 parameters measured to quantify firing patterns. ( B ) Fractional differences for the firing parameters showing a significant difference according to Wilk’s statistic for LPS versus vagus-dependent antidepressants and squalamine. Number of mice used were 6 for LPS (26 single units), 6 for JB-1 (23 single units), 3 for fluoxetine (11 single units), 7 for sertraline (29 single units), 3 for squalamine (12 single units), 10 for bupropion (44 single units) and 3 for LR6475 (12 single units). Panel ( C ) gives group (for all treatments) means and their combined Bonferroni confidence intervals. Intervals for BD and IBI did not straddle 0 indicating that both parameters in combination were responsible for the statistical difference given by Wilk’s statistic. ( D ) Significant difference between vagus-independent bupropion and vagus-dependent antidepressants. MII and GD in combination were responsible for this difference ( E ). ( F ) Non-antidepressant bacterium (LR6475) had significantly different firing parameters than the antidepressants. Only the MII parameter was responsible for generating this difference ( G ). ( H ) The intrinsic primary afferent neuron (IPAN) silencer DCEBIO (5 µM), the nicotinic receptor blocker mecamylamine (50 µM) or the ω-conotoxins GVIA and MVIIC (0.5 µM) disrupted the antidepressant code evoked by sertraline. No. of single units tested were 7 (2 mice) with DCEBIO, 6 (2 mice) with mecamylamine and 12 (3 mice) with conotoxins. I, MII, BD and GD together were responsible for the difference shown in ( H ). All mice were of the male BALB/c strain.

    Journal: Scientific Reports

    Article Title: Identification of SSRI-evoked antidepressant sensory signals by decoding vagus nerve activity

    doi: 10.1038/s41598-021-00615-w

    Figure Lengend Snippet: Vagus-dependent antidepressants had a unique spike firing pattern code that was disrupted by inhibition of IPAN to vagus synaptic transmission. ( A ) Diagram of stylised single unit discharge illustrating the 4 parameters measured to quantify firing patterns. ( B ) Fractional differences for the firing parameters showing a significant difference according to Wilk’s statistic for LPS versus vagus-dependent antidepressants and squalamine. Number of mice used were 6 for LPS (26 single units), 6 for JB-1 (23 single units), 3 for fluoxetine (11 single units), 7 for sertraline (29 single units), 3 for squalamine (12 single units), 10 for bupropion (44 single units) and 3 for LR6475 (12 single units). Panel ( C ) gives group (for all treatments) means and their combined Bonferroni confidence intervals. Intervals for BD and IBI did not straddle 0 indicating that both parameters in combination were responsible for the statistical difference given by Wilk’s statistic. ( D ) Significant difference between vagus-independent bupropion and vagus-dependent antidepressants. MII and GD in combination were responsible for this difference ( E ). ( F ) Non-antidepressant bacterium (LR6475) had significantly different firing parameters than the antidepressants. Only the MII parameter was responsible for generating this difference ( G ). ( H ) The intrinsic primary afferent neuron (IPAN) silencer DCEBIO (5 µM), the nicotinic receptor blocker mecamylamine (50 µM) or the ω-conotoxins GVIA and MVIIC (0.5 µM) disrupted the antidepressant code evoked by sertraline. No. of single units tested were 7 (2 mice) with DCEBIO, 6 (2 mice) with mecamylamine and 12 (3 mice) with conotoxins. I, MII, BD and GD together were responsible for the difference shown in ( H ). All mice were of the male BALB/c strain.

    Article Snippet: We tested the following “psychoactive” (change brain function or mood) agents: luminal administration of 109 cfu/mL live L. rhamnosus (JB-1), 10 µM sertraline hydrochloride (MilliporeSigma, Burlington, MA, USA) 30 µM fluoxetine hydrochloride (MilliporeSigma), 10 µM bupropion hydrochloride (MilliporeSigma) , or 1 mM LPS dissolved in pyrogen-free saline (Escherichia coli O127:B8, (MilliporeSigma) .

    Techniques: Inhibition, Transmission Assay, Mouse Assay

    The vagal firing pattern code for antidepressants in SW mice is comparable to that for BALB/c mice. ( A ) Effects of adding vagus-independent (bupropion) and vagus-dependent antidepressants in acute before and after experiments for jejunal segments taken from male Swiss Webster (SW) mice. There was a significant difference (Wilk’s Λ) in fractional differences for the 4 firing parameters between bupropion and the other antidepressants. ( B ) As was the case for BALB/c mice, MII and GD in combination were responsible for this difference. ( C , D ) Heat maps of the fractional differences illustrating the essential similarity of the antidepressant codes for SW and BALB/c mice.

    Journal: Scientific Reports

    Article Title: Identification of SSRI-evoked antidepressant sensory signals by decoding vagus nerve activity

    doi: 10.1038/s41598-021-00615-w

    Figure Lengend Snippet: The vagal firing pattern code for antidepressants in SW mice is comparable to that for BALB/c mice. ( A ) Effects of adding vagus-independent (bupropion) and vagus-dependent antidepressants in acute before and after experiments for jejunal segments taken from male Swiss Webster (SW) mice. There was a significant difference (Wilk’s Λ) in fractional differences for the 4 firing parameters between bupropion and the other antidepressants. ( B ) As was the case for BALB/c mice, MII and GD in combination were responsible for this difference. ( C , D ) Heat maps of the fractional differences illustrating the essential similarity of the antidepressant codes for SW and BALB/c mice.

    Article Snippet: We tested the following “psychoactive” (change brain function or mood) agents: luminal administration of 109 cfu/mL live L. rhamnosus (JB-1), 10 µM sertraline hydrochloride (MilliporeSigma, Burlington, MA, USA) 30 µM fluoxetine hydrochloride (MilliporeSigma), 10 µM bupropion hydrochloride (MilliporeSigma) , or 1 mM LPS dissolved in pyrogen-free saline (Escherichia coli O127:B8, (MilliporeSigma) .

    Techniques: Mouse Assay

    Paired differences graphs of mean interspike intervals before and after adding pro-, antidepressants or controls to the jejunal lumen. ( A – D ) vagus-dependent antidepressant agents (JB-1, sertraline and fluoxetine) and LPS decreased mean interspike intervals (MII) compared to paired Krebs control recordings. ( E – F ) Vagus-independent antidepressant bupropion increased MII and the non-antidepressant bacteria Lactobacillus reuteri ATCC PTA 6475 had little effect on MII. Effect sizes were calculated using the partial eta squared statistic η 2 p. Antidepressant agents produced a large effect, LPS a medium effect, and LR6475 had a small effect; see statistical analysis in “ Methods ”. Single unit numbers given above or below s.e.m, MII means given within solid bars.

    Journal: Scientific Reports

    Article Title: Identification of SSRI-evoked antidepressant sensory signals by decoding vagus nerve activity

    doi: 10.1038/s41598-021-00615-w

    Figure Lengend Snippet: Paired differences graphs of mean interspike intervals before and after adding pro-, antidepressants or controls to the jejunal lumen. ( A – D ) vagus-dependent antidepressant agents (JB-1, sertraline and fluoxetine) and LPS decreased mean interspike intervals (MII) compared to paired Krebs control recordings. ( E – F ) Vagus-independent antidepressant bupropion increased MII and the non-antidepressant bacteria Lactobacillus reuteri ATCC PTA 6475 had little effect on MII. Effect sizes were calculated using the partial eta squared statistic η 2 p. Antidepressant agents produced a large effect, LPS a medium effect, and LR6475 had a small effect; see statistical analysis in “ Methods ”. Single unit numbers given above or below s.e.m, MII means given within solid bars.

    Article Snippet: We tested the following “psychoactive” (change brain function or mood) agents: luminal administration of 109 cfu/mL live L. rhamnosus (JB-1), 10 µM sertraline hydrochloride (MilliporeSigma, Burlington, MA, USA) 30 µM fluoxetine hydrochloride (MilliporeSigma), 10 µM bupropion hydrochloride (MilliporeSigma) , or 1 mM LPS dissolved in pyrogen-free saline (Escherichia coli O127:B8, (MilliporeSigma) .

    Techniques: Produced

    The effect of fluoxetine (Panel ( A )), reboxetine (Panel ( B )), and bupropion (Panel ( C )) on antidepressant-like activity of HBK-10 in the forced swim test in mice. Studied compound and reference drugs: fluoxetine, reboxetine, and bupropion, were administered ip at sub-effective doses 30 min before the test. The results are presented as box plots showing the following data: mean (‘+’), median (horizontal line), upper and lower quartile (the width of the box shows interquartile range), upper and lower extreme (whiskers). Statistical analysis: Shapiro–Wilk test for normality, Brown–Forsythe test for homogeneity of variance, and two-way ANOVA (Newman–Keuls post hoc); ** p

    Journal: Pharmaceuticals

    Article Title: Synthesis and Evaluation of the Antidepressant-like Properties of HBK-10, a Novel 2-Methoxyphenylpiperazine Derivative Targeting the 5-HT1A and D2 Receptors

    doi: 10.3390/ph14080744

    Figure Lengend Snippet: The effect of fluoxetine (Panel ( A )), reboxetine (Panel ( B )), and bupropion (Panel ( C )) on antidepressant-like activity of HBK-10 in the forced swim test in mice. Studied compound and reference drugs: fluoxetine, reboxetine, and bupropion, were administered ip at sub-effective doses 30 min before the test. The results are presented as box plots showing the following data: mean (‘+’), median (horizontal line), upper and lower quartile (the width of the box shows interquartile range), upper and lower extreme (whiskers). Statistical analysis: Shapiro–Wilk test for normality, Brown–Forsythe test for homogeneity of variance, and two-way ANOVA (Newman–Keuls post hoc); ** p

    Article Snippet: HBK-10, WAY-100635 (Sigma, Darmstadt, Germany), p -chlorophenylalanine (p CPA; Sigma, Darmstadt, Germany), fluoxetine (Sigma, Darmstadt, Germany), reboxetine (Sigma, Darmstadt, Germany) and bupropion (Sigma, Darmstadt, Germany), were suspended in 1% Tween, and administered ip at a volume of 10 mL/kg 30 min before each behavioral test.

    Techniques: Activity Assay, Mouse Assay