nifedipine  (Thermo Fisher)


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    Structured Review

    Thermo Fisher nifedipine
    CYP1A2- and CYP3A11-mediated metabolism (generation of paracetamol and oxidized <t>nifedipine,</t> respectively) in mouse liver microsomes from the treated (induced by plumbagin for 28 days) and the control groups. Data are expressed as median (interquartile range) from 3 male mice
    Nifedipine, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nifedipine/product/Thermo Fisher
    Average 91 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2021-01
    91/100 stars

    Images

    1) Product Images from "Pharmacokinetics, toxicity, and cytochrome P450 modulatory activity of plumbagin"

    Article Title: Pharmacokinetics, toxicity, and cytochrome P450 modulatory activity of plumbagin

    Journal: BMC Pharmacology & Toxicology

    doi: 10.1186/s40360-016-0094-5

    CYP1A2- and CYP3A11-mediated metabolism (generation of paracetamol and oxidized nifedipine, respectively) in mouse liver microsomes from the treated (induced by plumbagin for 28 days) and the control groups. Data are expressed as median (interquartile range) from 3 male mice
    Figure Legend Snippet: CYP1A2- and CYP3A11-mediated metabolism (generation of paracetamol and oxidized nifedipine, respectively) in mouse liver microsomes from the treated (induced by plumbagin for 28 days) and the control groups. Data are expressed as median (interquartile range) from 3 male mice

    Techniques Used: Mouse Assay

    2) Product Images from "Functional link between muscarinic receptors and large-conductance Ca2+-activated K+ channels in freshly-isolated human detrusor smooth muscle cells"

    Article Title: Functional link between muscarinic receptors and large-conductance Ca2+-activated K+ channels in freshly-isolated human detrusor smooth muscle cells

    Journal: Pflugers Archiv : European journal of physiology

    doi: 10.1007/s00424-014-1537-8

    mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and nifedipine (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and
    Figure Legend Snippet: mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and nifedipine (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and

    Techniques Used: Inhibition, Activation Assay, Isolation, Transferring

    3) Product Images from "Nifedipine Treatment Reduces Resting Calcium Concentration, Oxidative and Apoptotic Gene Expression, and Improves Muscle Function in Dystrophic mdx Mice"

    Article Title: Nifedipine Treatment Reduces Resting Calcium Concentration, Oxidative and Apoptotic Gene Expression, and Improves Muscle Function in Dystrophic mdx Mice

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0081222

    Nifedipine treatment reduces muscle [Ca 2+ ] r in vivo in mdx mice. Mice were treated with daily intraperitoneal injections of nifedipine 1/Kg for 1-week or saline. A. Experimental setup to measure [Ca 2+ ] r in vivo with Ca 2+ selective microelectrodes in vastus lateralis muscle. B. Averaged data from [Ca 2+ ] r determinations with or without nifedipine treatment. Data are expressed as mean ± S.E.M. from n fibers in N mice, *** P
    Figure Legend Snippet: Nifedipine treatment reduces muscle [Ca 2+ ] r in vivo in mdx mice. Mice were treated with daily intraperitoneal injections of nifedipine 1/Kg for 1-week or saline. A. Experimental setup to measure [Ca 2+ ] r in vivo with Ca 2+ selective microelectrodes in vastus lateralis muscle. B. Averaged data from [Ca 2+ ] r determinations with or without nifedipine treatment. Data are expressed as mean ± S.E.M. from n fibers in N mice, *** P

    Techniques Used: In Vivo, Mouse Assay

    NF-κB activity and iNOS expression in both wt and mdx myotubes. A. NF-κB activity was studied with a luciferase reporter. Nifedipine treatment (10 µM for 6 h) reduced NF-κB activity in mdx , without any significant effect in wt myotubes (n = 6–12). B. mRNA levels of iNOS were determined by real time PCR after 6 h of nifedipine treatment (10 µM) (n = 6–7). Data are expressed as mean ± S.E.M., * P
    Figure Legend Snippet: NF-κB activity and iNOS expression in both wt and mdx myotubes. A. NF-κB activity was studied with a luciferase reporter. Nifedipine treatment (10 µM for 6 h) reduced NF-κB activity in mdx , without any significant effect in wt myotubes (n = 6–12). B. mRNA levels of iNOS were determined by real time PCR after 6 h of nifedipine treatment (10 µM) (n = 6–7). Data are expressed as mean ± S.E.M., * P

    Techniques Used: Activity Assay, Expressing, Luciferase, Real-time Polymerase Chain Reaction

    Bax and BIM gene expression in diaphragm muscles. Diaphragms were dissected from nifedipine- and saline-treated mice and mRNA levels were assessed by real time PCR. A. Bax, B. BIM mRNA levels. Data are expressed as mean ± S.E.M. Diaphragms were obtained from n = mice as indicated in the figure, * P
    Figure Legend Snippet: Bax and BIM gene expression in diaphragm muscles. Diaphragms were dissected from nifedipine- and saline-treated mice and mRNA levels were assessed by real time PCR. A. Bax, B. BIM mRNA levels. Data are expressed as mean ± S.E.M. Diaphragms were obtained from n = mice as indicated in the figure, * P

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction

    Extracellular ATP concentration in FDB fibers isolated from either nifedipine- or saline-treated wt and mdx mice. A. Time course of extracellular ATP levels after media change. ATP concentration was measured with CellTiter-Glo® Luminescent Cell Viability Assay. Average extracellular ATP at 30 min ( B ) and at 39 min ( C ) after media change are shown in the figure. Data are expressed as mean ± S.E.M. FDB fibers were cultured from n = mice are indicated in the figure. ** P
    Figure Legend Snippet: Extracellular ATP concentration in FDB fibers isolated from either nifedipine- or saline-treated wt and mdx mice. A. Time course of extracellular ATP levels after media change. ATP concentration was measured with CellTiter-Glo® Luminescent Cell Viability Assay. Average extracellular ATP at 30 min ( B ) and at 39 min ( C ) after media change are shown in the figure. Data are expressed as mean ± S.E.M. FDB fibers were cultured from n = mice are indicated in the figure. ** P

    Techniques Used: Concentration Assay, Isolation, Mouse Assay, Cell Viability Assay, Cell Culture

    Nifedipine incubation reduces [Ca 2+ ] r in mdx myotubes. Myotubes were incubated with 10 µM Nifedipine for 10 min at room temperature in Krebs Ringer solution and [Ca 2+ ] r was measured using double-barreled Ca 2+ selective microelectrodes. Data are expressed as mean ± S.E.M. Wt (n = 10), mdx (n = 27), Wt +Nife (n = 10) and mdx+ Nife (n = 10). *** P
    Figure Legend Snippet: Nifedipine incubation reduces [Ca 2+ ] r in mdx myotubes. Myotubes were incubated with 10 µM Nifedipine for 10 min at room temperature in Krebs Ringer solution and [Ca 2+ ] r was measured using double-barreled Ca 2+ selective microelectrodes. Data are expressed as mean ± S.E.M. Wt (n = 10), mdx (n = 27), Wt +Nife (n = 10) and mdx+ Nife (n = 10). *** P

    Techniques Used: Incubation

    Proposed model for ATP-mediated effects in dystrophic skeletal muscle. In dystrophic skeletal muscle fibers there is an increase in basal ATP release, through Pannexin1 channels that is modulated by the DHPR [12] . Extracellular ATP increases the [Ca 2+ ] r in dystrophic muscle fibers through the activation of purinergic receptors (P 2 X, inotropic and P 2 Y, metabotropic). This leads to the expression of pro-apoptotic and pro-inflammatory genes, increasing the muscle damage observed in dystrophic skeletal muscle cells. Nifedipine treatment reduces the basal ATP release and reduces [Ca 2+ ] r, resulting in less pro-inflammatory and pro-apoptotic gene expression and subsequently reduces muscle damage as indicated by a decrease in blood CK and an increase in muscle function assessed by the inverted grid-hanging test and the force swimming test.
    Figure Legend Snippet: Proposed model for ATP-mediated effects in dystrophic skeletal muscle. In dystrophic skeletal muscle fibers there is an increase in basal ATP release, through Pannexin1 channels that is modulated by the DHPR [12] . Extracellular ATP increases the [Ca 2+ ] r in dystrophic muscle fibers through the activation of purinergic receptors (P 2 X, inotropic and P 2 Y, metabotropic). This leads to the expression of pro-apoptotic and pro-inflammatory genes, increasing the muscle damage observed in dystrophic skeletal muscle cells. Nifedipine treatment reduces the basal ATP release and reduces [Ca 2+ ] r, resulting in less pro-inflammatory and pro-apoptotic gene expression and subsequently reduces muscle damage as indicated by a decrease in blood CK and an increase in muscle function assessed by the inverted grid-hanging test and the force swimming test.

    Techniques Used: Activation Assay, Expressing

    Nifedipine treatment reduced serum CK and increases muscle function in mdx mice. A. Blood samples were collected by cardiac puncture under anesthesia from both nifedipine- or saline-treated mice. CK activities were determined by the UV kinetic method. B. Averaged hanging time obtained in the inverted grid-hanging test in saline- and nifedipine treated mice. C. Averaged swimming time obtained in the forced swimming test in nifedipine- or saline- treated mdx mice. Data are expressed as mean ± S.E.M. n = mice is indicated in the figure, * P
    Figure Legend Snippet: Nifedipine treatment reduced serum CK and increases muscle function in mdx mice. A. Blood samples were collected by cardiac puncture under anesthesia from both nifedipine- or saline-treated mice. CK activities were determined by the UV kinetic method. B. Averaged hanging time obtained in the inverted grid-hanging test in saline- and nifedipine treated mice. C. Averaged swimming time obtained in the forced swimming test in nifedipine- or saline- treated mdx mice. Data are expressed as mean ± S.E.M. n = mice is indicated in the figure, * P

    Techniques Used: Mouse Assay

    iNOS and NADPH oxidase subunits gene expression in diaphragm muscles. Diaphragms were dissected from nifedipine- and saline-treated mice and mRNA levels were assessed by real time PCR. A. iNOS, B. , gp91 phox and C. p47 phox expression. Data are expressed as mean ± S.E.M. Diaphragms were obtained from n = mice as indicated in the figure. * P
    Figure Legend Snippet: iNOS and NADPH oxidase subunits gene expression in diaphragm muscles. Diaphragms were dissected from nifedipine- and saline-treated mice and mRNA levels were assessed by real time PCR. A. iNOS, B. , gp91 phox and C. p47 phox expression. Data are expressed as mean ± S.E.M. Diaphragms were obtained from n = mice as indicated in the figure. * P

    Techniques Used: Expressing, Mouse Assay, Real-time Polymerase Chain Reaction

    4) Product Images from "Bryophyllum pinnatum enhances the inhibitory effect of atosiban and nifedipine on human myometrial contractility: an in vitro study"

    Article Title: Bryophyllum pinnatum enhances the inhibitory effect of atosiban and nifedipine on human myometrial contractility: an in vitro study

    Journal: BMC Complementary and Alternative Medicine

    doi: 10.1186/s12906-019-2711-5

    Effect of BPJ, atosiban, nifedipine, BPJ plus atosiban and BPJ plus nifedipine on myometrium cell viability. ( a ) Cell viability assays were performed in the presence of BPJ (2.5–10.0 μg/mL), atosiban (0.3–1.1 μg/mL) and nifedipine (3.0–12.0 ng/mL), as well as of BPJ plus atosiban and BPJ plus nifedipine (same concentrations as with single treatments) using hTERT-C3 and PHM1–41 human myometrium cell lines. Cells were incubated with the test substances for 24 h. Triton X-100 (1%) and ethyl methanesulfonate (30 mM) were used as positive controls. Data is presented as mean ± SEM of 4 independent experiments ( n = 4), each carried out in quadruplicate; * p
    Figure Legend Snippet: Effect of BPJ, atosiban, nifedipine, BPJ plus atosiban and BPJ plus nifedipine on myometrium cell viability. ( a ) Cell viability assays were performed in the presence of BPJ (2.5–10.0 μg/mL), atosiban (0.3–1.1 μg/mL) and nifedipine (3.0–12.0 ng/mL), as well as of BPJ plus atosiban and BPJ plus nifedipine (same concentrations as with single treatments) using hTERT-C3 and PHM1–41 human myometrium cell lines. Cells were incubated with the test substances for 24 h. Triton X-100 (1%) and ethyl methanesulfonate (30 mM) were used as positive controls. Data is presented as mean ± SEM of 4 independent experiments ( n = 4), each carried out in quadruplicate; * p

    Techniques Used: Incubation

    Experimental design for measurement of myometrial contractions. Test substances were added to the organ bath when myometrium strips had been contracting regularly for 30 min. When the effects of BPJ and/or atosiban were being studied ( a ) , Krebs solution (control), BPJ, atosiban, or the combination of BPJ and atosiban were added, and contractility was recorded for 30 min. When the effects of BPJ and/or nifedipine were being studied ( b ) , Krebs solution (control; two strips) or nifedipine (two strips) was added, contractility was recorded for 30 min, and then BPJ was added to all chambers. Exposure to test substances was followed by a 30 min washout step, with change of Krebs solution at 5, 10, 20 and 30 min
    Figure Legend Snippet: Experimental design for measurement of myometrial contractions. Test substances were added to the organ bath when myometrium strips had been contracting regularly for 30 min. When the effects of BPJ and/or atosiban were being studied ( a ) , Krebs solution (control), BPJ, atosiban, or the combination of BPJ and atosiban were added, and contractility was recorded for 30 min. When the effects of BPJ and/or nifedipine were being studied ( b ) , Krebs solution (control; two strips) or nifedipine (two strips) was added, contractility was recorded for 30 min, and then BPJ was added to all chambers. Exposure to test substances was followed by a 30 min washout step, with change of Krebs solution at 5, 10, 20 and 30 min

    Techniques Used:

    Effect of BPJ, nifedipine, and the combination of BPJ with nifedipine on human myometrial contractility in vitro. BPJ (green; 15 μL), nifedipine (violet; 5 μL of 3.7 μg/mL), or their combination (orange, same concentrations) were added to the myograph chamber. The scatter dot plot shows the AUC ( a ), the amplitude ( b ), and the frequency ( c ) expressed as percentage of initial. Krebs solution was used as negative control (black, 5 μL). Data were obtained from 11 to 13 different biopsies (n = 11–13) and are presented as mean value ± SEM. *p
    Figure Legend Snippet: Effect of BPJ, nifedipine, and the combination of BPJ with nifedipine on human myometrial contractility in vitro. BPJ (green; 15 μL), nifedipine (violet; 5 μL of 3.7 μg/mL), or their combination (orange, same concentrations) were added to the myograph chamber. The scatter dot plot shows the AUC ( a ), the amplitude ( b ), and the frequency ( c ) expressed as percentage of initial. Krebs solution was used as negative control (black, 5 μL). Data were obtained from 11 to 13 different biopsies (n = 11–13) and are presented as mean value ± SEM. *p

    Techniques Used: In Vitro, Negative Control

    Effect of repeated addition of BPJ plus atosiban (15 μL and 4.3 μL of 375 μg/mL, respectively) and of BPJ plus nifedipine (15 μL and 5 μL of 3.7 μg/mL, respectively) on human myometrial contractility in vitro. All test substances were repeatedly added to the myograph chamber. The line chart shows the AUC ( a ), the amplitude ( b ), and the frequency ( c ). Data were obtained with 5 different biopsies ( n = 5) and are expressed as percentage of initial. The repeated addition of BPJ was performed for comparison; Krebs solution (5 μL) was used as control. * p
    Figure Legend Snippet: Effect of repeated addition of BPJ plus atosiban (15 μL and 4.3 μL of 375 μg/mL, respectively) and of BPJ plus nifedipine (15 μL and 5 μL of 3.7 μg/mL, respectively) on human myometrial contractility in vitro. All test substances were repeatedly added to the myograph chamber. The line chart shows the AUC ( a ), the amplitude ( b ), and the frequency ( c ). Data were obtained with 5 different biopsies ( n = 5) and are expressed as percentage of initial. The repeated addition of BPJ was performed for comparison; Krebs solution (5 μL) was used as control. * p

    Techniques Used: In Vitro

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    Article Snippet: Materials Acetylcholine chloride (ACh), phenylephrine hydrochloride (PE), and nifedipine were purchased from Acros Organics (Geel, Belgium).

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    Thermo Fisher nifedipine
    mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and <t>nifedipine</t> (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and
    Nifedipine, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nifedipine/product/Thermo Fisher
    Average 91 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    nifedipine - by Bioz Stars, 2021-01
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    mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and nifedipine (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and

    Journal: Pflugers Archiv : European journal of physiology

    Article Title: Functional link between muscarinic receptors and large-conductance Ca2+-activated K+ channels in freshly-isolated human detrusor smooth muscle cells

    doi: 10.1007/s00424-014-1537-8

    Figure Lengend Snippet: mAChR agonist carbachol does not affect the depolarization-induced whole cell steady-state K Ca 1.1 currents under conditions of pharmacological inhibition of the major cellular sources of Ca 2+ for K Ca 1.1 channel activation in freshly-isolated human DSM cells A) Representative original recordings illustrate the depolarization-induced whole cell steady-state K Ca 1.1 currents in the absence (control) and in the presence of carbachol (1 μM). B) The current-voltage relationship curve summarizes the lack of carbachol effects on the whole cell steady-state K Ca 1.1 currents (n=9, N=6; P > 0.05). Steady-state K Ca 1.1 currents were recorded in the presence of ryanodine (30 μM), thapsigargin (100 nM), and nifedipine (1 μM). The bath solution contained 134 mM NaCl, 6 mM KCl, and 2 mM CaCl 2 , and the pipette 110 mM potassium aspartate, 30 mM KCl, 10 mM NaCl, and

    Article Snippet: Stock solutions of ryanodine (Enzo Life Sciences, Inc.,NY), nifedipine (Thermo Fisher Scientific, NJ), thapsigargin (MP Biochemicals, LLC, CA), and paxilline (Sigma) were prepared in DMSO or ethanol.

    Techniques: Inhibition, Activation Assay, Isolation, Transferring