Structured Review

Proteintech nox2 19013
Nox2 19013, supplied by Proteintech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews
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nox2 19013 - by Bioz Stars, 2024-07
86/100 stars

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Proteintech nox2 19013
Protein expression in different doses of S protein induced HUVECs. A . ACE2 and TMPRSS2 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. B . Relative expression of gray values for ACE2. C . Relative expression of gray values for TMPRSS2. D . NOX1 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. E . Relative expression of gray values for NOX1. F . <t>NOX2</t> protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. G . Relative expression of gray values for NOX2. H . NOX3 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. I . Relative expression of gray values for NOX3. J . NOX4 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. K . Relative expression of gray values for NOX4
Nox2 19013, supplied by Proteintech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nox2 19013/product/Proteintech
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
nox2 19013 - by Bioz Stars, 2024-07
86/100 stars

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1) Product Images from "Synergistic effect of elevated glucose levels with SARS-CoV-2 spike protein induced NOX-dependent ROS production in endothelial cells"

Article Title: Synergistic effect of elevated glucose levels with SARS-CoV-2 spike protein induced NOX-dependent ROS production in endothelial cells

Journal: Molecular Biology Reports

doi: 10.1007/s11033-023-08504-3

Protein expression in different doses of S protein induced HUVECs. A . ACE2 and TMPRSS2 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. B . Relative expression of gray values for ACE2. C . Relative expression of gray values for TMPRSS2. D . NOX1 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. E . Relative expression of gray values for NOX1. F . NOX2 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. G . Relative expression of gray values for NOX2. H . NOX3 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. I . Relative expression of gray values for NOX3. J . NOX4 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. K . Relative expression of gray values for NOX4
Figure Legend Snippet: Protein expression in different doses of S protein induced HUVECs. A . ACE2 and TMPRSS2 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. B . Relative expression of gray values for ACE2. C . Relative expression of gray values for TMPRSS2. D . NOX1 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. E . Relative expression of gray values for NOX1. F . NOX2 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. G . Relative expression of gray values for NOX2. H . NOX3 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. I . Relative expression of gray values for NOX3. J . NOX4 protein expression relative to GAPDH analyzed by western blot in different doses of S protein induced HUVECs. K . Relative expression of gray values for NOX4

Techniques Used: Expressing, Western Blot


Structured Review

Proteintech anti nox 2
Anti Nox 2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews
Price from $9.99 to $1999.99
anti nox 2 - by Bioz Stars, 2024-07
94/100 stars

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Proteintech anti gp91 phox
Anti Gp91 Phox, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti gp91 phox/product/Proteintech
Average 94 stars, based on 1 article reviews
Price from $9.99 to $1999.99
anti gp91 phox - by Bioz Stars, 2024-07
94/100 stars

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Proteintech nox2
AUDA administration alleviated cardiac dysfunction and reduced apoptosis in db/db mice heart. (a) Representative immunoblots and quantitation of soluble epoxide hydrolase (sEH) expression, (b) +dp/dt max, (c) -dp/dt min, (d) left ventricular ejection fraction (LVEF), (e) left ventricular internal diameter end systole (LVID(s)), (f) left ventricular internal diameter end diastole (LVID(d)), and (g) E/A ratio. (h and i) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, <t>NOX2,</t> and SOD1 in the myocardia of mice treated with or without the sEH inhibitor AUDA. (j and k) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (l–o) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia in different groups. Data were expressed as mean ± SEM ( n = 8 mice per group). ∗ p < 0.05 vs. Con and # p < 0.05 vs. DM or HGHF. Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; MABSA: mannitol+ BSA; DHE: dihydroethidium; HGHF: high glucose and high fat.
Nox2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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94/100 stars

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1) Product Images from "Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation"

Article Title: Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2022/3773415

AUDA administration alleviated cardiac dysfunction and reduced apoptosis in db/db mice heart. (a) Representative immunoblots and quantitation of soluble epoxide hydrolase (sEH) expression, (b) +dp/dt max, (c) -dp/dt min, (d) left ventricular ejection fraction (LVEF), (e) left ventricular internal diameter end systole (LVID(s)), (f) left ventricular internal diameter end diastole (LVID(d)), and (g) E/A ratio. (h and i) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice treated with or without the sEH inhibitor AUDA. (j and k) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (l–o) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia in different groups. Data were expressed as mean ± SEM ( n = 8 mice per group). ∗ p < 0.05 vs. Con and # p < 0.05 vs. DM or HGHF. Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; MABSA: mannitol+ BSA; DHE: dihydroethidium; HGHF: high glucose and high fat.
Figure Legend Snippet: AUDA administration alleviated cardiac dysfunction and reduced apoptosis in db/db mice heart. (a) Representative immunoblots and quantitation of soluble epoxide hydrolase (sEH) expression, (b) +dp/dt max, (c) -dp/dt min, (d) left ventricular ejection fraction (LVEF), (e) left ventricular internal diameter end systole (LVID(s)), (f) left ventricular internal diameter end diastole (LVID(d)), and (g) E/A ratio. (h and i) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice treated with or without the sEH inhibitor AUDA. (j and k) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (l–o) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia in different groups. Data were expressed as mean ± SEM ( n = 8 mice per group). ∗ p < 0.05 vs. Con and # p < 0.05 vs. DM or HGHF. Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; MABSA: mannitol+ BSA; DHE: dihydroethidium; HGHF: high glucose and high fat.

Techniques Used: Western Blot, Quantitation Assay, Expressing, TUNEL Assay, Staining

Small interfering RNA of Nrf2 specifically reduced the protective effects of AUDA on cardiomyocytes autophagy and apoptosis. (a and b) Representative immunoblots and quantitation of protein expression of Beclin 1, Atg3, and LC3II in HGHF-stimulated cardiomyocytes in different groups. (c) LC3-II/ β -actin ratio with or without bafilomycin A1 treatment under HGHF culture conditions. (d and e) Representative images of fluorescent LC3 puncta and quantitation of cardiomyocytes with different treatments. (f and g) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (h and i) Representative images and quantitation of cardiomyocyte apoptosis via the Annexin-V/PI apoptotic assay. (j and k) Representative images and quantitation of cardiomyocyte ROS levels via DCFH-DA. Data were expressed as mean ± SEM (n ≥ 3 per group). ∗ p < 0.05 vs. si-Con+Con and # p < 0.05 vs. si-Nrf2+Con. HGHF: high glucose and high fat.
Figure Legend Snippet: Small interfering RNA of Nrf2 specifically reduced the protective effects of AUDA on cardiomyocytes autophagy and apoptosis. (a and b) Representative immunoblots and quantitation of protein expression of Beclin 1, Atg3, and LC3II in HGHF-stimulated cardiomyocytes in different groups. (c) LC3-II/ β -actin ratio with or without bafilomycin A1 treatment under HGHF culture conditions. (d and e) Representative images of fluorescent LC3 puncta and quantitation of cardiomyocytes with different treatments. (f and g) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (h and i) Representative images and quantitation of cardiomyocyte apoptosis via the Annexin-V/PI apoptotic assay. (j and k) Representative images and quantitation of cardiomyocyte ROS levels via DCFH-DA. Data were expressed as mean ± SEM (n ≥ 3 per group). ∗ p < 0.05 vs. si-Con+Con and # p < 0.05 vs. si-Nrf2+Con. HGHF: high glucose and high fat.

Techniques Used: Small Interfering RNA, Western Blot, Quantitation Assay, Expressing

Virus carrying code for Nrf2 shRNA specifically reduced the protective effects of AUDA on apoptosis in db/db mice heart. (a and b) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice from different groups. (c–f) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia from different groups. (g) Mechanism diagram of full text. Data were expressed as mean ± SEM (n = 8 per group). ∗ p < 0.05 vs. ScshRNA +Con, # p < 0.05 vs. Nrf2shRNA+Con, and & p < 0.05 vs. Nrf2shRNA+DM. ScshRNA: AAV-ScshRNA; Nrf2shRNA: AAV-Nrf2shRNA; Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; DHE: dihydroethidium.
Figure Legend Snippet: Virus carrying code for Nrf2 shRNA specifically reduced the protective effects of AUDA on apoptosis in db/db mice heart. (a and b) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice from different groups. (c–f) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia from different groups. (g) Mechanism diagram of full text. Data were expressed as mean ± SEM (n = 8 per group). ∗ p < 0.05 vs. ScshRNA +Con, # p < 0.05 vs. Nrf2shRNA+Con, and & p < 0.05 vs. Nrf2shRNA+DM. ScshRNA: AAV-ScshRNA; Nrf2shRNA: AAV-Nrf2shRNA; Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; DHE: dihydroethidium.

Techniques Used: shRNA, Western Blot, Quantitation Assay, Expressing, TUNEL Assay, Staining


Structured Review

Proteintech anti nox2
VEGFR-3 knockdown accelerates Ang II-induced cardiac fibrosis, oxidative stress, and inflammation in mice. VEGFR-3 f/f and Lyve-1 Cre VEGFR-3 f/− mice were infused with saline or Ang II (1000 ng/kg/min) for 14 days. (a) Cardiac Masson staining (left) and quantitative analysis of the fibrotic area (%) (right, n = 6). (b) qPCR analyses of myocardial collagen I and collagen III levels ( n = 6). (c) Cardiac α -SMA immunohistochemical staining (left) and quantitative analysis of the positive area (right, n = 6). (d) qPCR analyses of myocardial α -SMA levels ( n = 6). (e) Cardiac DHE fluorescence staining (left) and quantitative analysis of relative fluorescence intensity (right, n = 6). (f) qPCR analyses of myocardial <t>NOX2</t> and NOX4 levels ( n = 6). (g) CD68 (red) and DAPI (blue) fluorescence staining of heart sections (left) and quantification of CD68 + macrophages (right, n = 6). (h) qPCR analyses of myocardial IL-1 β and IL-6 levels ( n = 6). (i) Immunoblot analysis of cardiac TGF- β 1, p-Smad2/3, Smad2/3, NOX2, NOX4, p-P65, and P65 levels (left) and quantification (right, n = 4). The data are presented as the mean ± SD; n represents the number of animals in each group. Statistical differences were determined by two-way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the VEGFR-3 f/f +saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the VEGFR-3 f/f +Ang II group.
Anti Nox2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti nox2 - by Bioz Stars, 2024-07
94/100 stars

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1) Product Images from "Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms"

Article Title: Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2022/5044046

VEGFR-3 knockdown accelerates Ang II-induced cardiac fibrosis, oxidative stress, and inflammation in mice. VEGFR-3 f/f and Lyve-1 Cre VEGFR-3 f/− mice were infused with saline or Ang II (1000 ng/kg/min) for 14 days. (a) Cardiac Masson staining (left) and quantitative analysis of the fibrotic area (%) (right, n = 6). (b) qPCR analyses of myocardial collagen I and collagen III levels ( n = 6). (c) Cardiac α -SMA immunohistochemical staining (left) and quantitative analysis of the positive area (right, n = 6). (d) qPCR analyses of myocardial α -SMA levels ( n = 6). (e) Cardiac DHE fluorescence staining (left) and quantitative analysis of relative fluorescence intensity (right, n = 6). (f) qPCR analyses of myocardial NOX2 and NOX4 levels ( n = 6). (g) CD68 (red) and DAPI (blue) fluorescence staining of heart sections (left) and quantification of CD68 + macrophages (right, n = 6). (h) qPCR analyses of myocardial IL-1 β and IL-6 levels ( n = 6). (i) Immunoblot analysis of cardiac TGF- β 1, p-Smad2/3, Smad2/3, NOX2, NOX4, p-P65, and P65 levels (left) and quantification (right, n = 4). The data are presented as the mean ± SD; n represents the number of animals in each group. Statistical differences were determined by two-way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the VEGFR-3 f/f +saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the VEGFR-3 f/f +Ang II group.
Figure Legend Snippet: VEGFR-3 knockdown accelerates Ang II-induced cardiac fibrosis, oxidative stress, and inflammation in mice. VEGFR-3 f/f and Lyve-1 Cre VEGFR-3 f/− mice were infused with saline or Ang II (1000 ng/kg/min) for 14 days. (a) Cardiac Masson staining (left) and quantitative analysis of the fibrotic area (%) (right, n = 6). (b) qPCR analyses of myocardial collagen I and collagen III levels ( n = 6). (c) Cardiac α -SMA immunohistochemical staining (left) and quantitative analysis of the positive area (right, n = 6). (d) qPCR analyses of myocardial α -SMA levels ( n = 6). (e) Cardiac DHE fluorescence staining (left) and quantitative analysis of relative fluorescence intensity (right, n = 6). (f) qPCR analyses of myocardial NOX2 and NOX4 levels ( n = 6). (g) CD68 (red) and DAPI (blue) fluorescence staining of heart sections (left) and quantification of CD68 + macrophages (right, n = 6). (h) qPCR analyses of myocardial IL-1 β and IL-6 levels ( n = 6). (i) Immunoblot analysis of cardiac TGF- β 1, p-Smad2/3, Smad2/3, NOX2, NOX4, p-P65, and P65 levels (left) and quantification (right, n = 4). The data are presented as the mean ± SD; n represents the number of animals in each group. Statistical differences were determined by two-way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the VEGFR-3 f/f +saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the VEGFR-3 f/f +Ang II group.

Techniques Used: Staining, Immunohistochemical staining, Fluorescence, Western Blot


Structured Review

Proteintech nox2
Oxidative stress in the aorta in response to acute and recurrent hypoglycemia in aged T2DM rats. <t>NOX2/4</t> expression was assayed by (a) western blotting, (b) serum levels of SOD, (c) GSH-Px, and (d) MDA were tested. (e) 8-OHdG location and expression were determined by immunofluorescence; ∗ p < 0.05 DM vs. control; # p < 0.05 H-DM, RH-DM vs. DM; & p < 0.05 H-DM vs. RH-DM.
Nox2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nox2/product/Proteintech
Average 94 stars, based on 1 article reviews
Price from $9.99 to $1999.99
nox2 - by Bioz Stars, 2024-07
94/100 stars

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1) Product Images from "Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis"

Article Title: Recurrent Hypoglycemia Impaired Vascular Function in Advanced T2DM Rats by Inducing Pyroptosis

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2022/7812407

Oxidative stress in the aorta in response to acute and recurrent hypoglycemia in aged T2DM rats. NOX2/4 expression was assayed by (a) western blotting, (b) serum levels of SOD, (c) GSH-Px, and (d) MDA were tested. (e) 8-OHdG location and expression were determined by immunofluorescence; ∗ p < 0.05 DM vs. control; # p < 0.05 H-DM, RH-DM vs. DM; & p < 0.05 H-DM vs. RH-DM.
Figure Legend Snippet: Oxidative stress in the aorta in response to acute and recurrent hypoglycemia in aged T2DM rats. NOX2/4 expression was assayed by (a) western blotting, (b) serum levels of SOD, (c) GSH-Px, and (d) MDA were tested. (e) 8-OHdG location and expression were determined by immunofluorescence; ∗ p < 0.05 DM vs. control; # p < 0.05 H-DM, RH-DM vs. DM; & p < 0.05 H-DM vs. RH-DM.

Techniques Used: Expressing, Western Blot, Immunofluorescence


Structured Review

Proteintech gp91 phox
Treatment of LXA4 inhibits oxidative stress in corpus cavernous of DMED rats. ( a ) Representative Western blot results for the p22 <t>phox</t> , p47 phox , <t>gp91</t> phox , p40 phox , and p67 phox in rats of all the three groups. ( b ) Expressions of p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox with β-actin as the loading control in all the three groups were presented through bar graphs. ( c ) MDA levels determined by the ELISA method in all the three groups. ( d ) SOD activities determined by the ELISA method in all the three groups. Data are expressed as mean ± s.e.m. ( n control = 10, n DMED = 11, and n DMED + LXA4 = 11). * P < 0.05 and *** P < 0.001 when comparing two groups. DMED: diabetes mellitus-induced erectile dysfunction; LXA4: Lipoxin A4; ELISA: enzyme-linked immunosorbent assay; SOD: superoxide dismutase; MDA: malondialdehyde; s.e.m.: standard error of the mean.
Gp91 Phox, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Price from $9.99 to $1999.99
gp91 phox - by Bioz Stars, 2024-07
94/100 stars

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1) Product Images from "Lipoxin A4 improves erectile dysfunction in rats with type I diabetes by inhibiting oxidative stress and corporal fibrosis"

Article Title: Lipoxin A4 improves erectile dysfunction in rats with type I diabetes by inhibiting oxidative stress and corporal fibrosis

Journal: Asian Journal of Andrology

doi: 10.4103/aja.aja_49_17

Treatment of LXA4 inhibits oxidative stress in corpus cavernous of DMED rats. ( a ) Representative Western blot results for the p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox in rats of all the three groups. ( b ) Expressions of p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox with β-actin as the loading control in all the three groups were presented through bar graphs. ( c ) MDA levels determined by the ELISA method in all the three groups. ( d ) SOD activities determined by the ELISA method in all the three groups. Data are expressed as mean ± s.e.m. ( n control = 10, n DMED = 11, and n DMED + LXA4 = 11). * P < 0.05 and *** P < 0.001 when comparing two groups. DMED: diabetes mellitus-induced erectile dysfunction; LXA4: Lipoxin A4; ELISA: enzyme-linked immunosorbent assay; SOD: superoxide dismutase; MDA: malondialdehyde; s.e.m.: standard error of the mean.
Figure Legend Snippet: Treatment of LXA4 inhibits oxidative stress in corpus cavernous of DMED rats. ( a ) Representative Western blot results for the p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox in rats of all the three groups. ( b ) Expressions of p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox with β-actin as the loading control in all the three groups were presented through bar graphs. ( c ) MDA levels determined by the ELISA method in all the three groups. ( d ) SOD activities determined by the ELISA method in all the three groups. Data are expressed as mean ± s.e.m. ( n control = 10, n DMED = 11, and n DMED + LXA4 = 11). * P < 0.05 and *** P < 0.001 when comparing two groups. DMED: diabetes mellitus-induced erectile dysfunction; LXA4: Lipoxin A4; ELISA: enzyme-linked immunosorbent assay; SOD: superoxide dismutase; MDA: malondialdehyde; s.e.m.: standard error of the mean.

Techniques Used: Western Blot, Enzyme-linked Immunosorbent Assay


Structured Review

Proteintech nadph oxidase 2
Higher Slc26a6 expression induced more intracellular ROS generation by oxalate. (a) Four cell types were stimulated with oxalate (700 μ M) for 3 h, and intracellular ROS levels were determined by fluorescence intensity of DCFH analyzed using flow cytometry. Changes before and after oxalate treatment are shown on the right graph as means ± SD ( n = 3). ∗ P < 0.05. (b) Lipid peroxidation was assessed by detecting the MDA level in supernatants of NRK cell lysates. NRK-Slc26a6 cells showed an obvious increase in MDA generation compared with control groups after oxalate treatment ( n = 6). (c) Activity change of superoxide dismutase (SOD) expressed as means ± SD. In the NRK-Slc26a6 group, SOD activity was markedly decreased compared to that in control groups. (d, e, f) Expressions of NADPH <t>oxidase</t> <t>2</t> <t>(Nox2)</t> and Nox4 before and after oxalate treatment in all groups using Western blot analysis. After oxalate treatment (700 μ M) for 24 h, the expression of Nox4 increased in the NRK-Slc26a6 group and that of Nox2 was decreased in the NRK-siRNA group. Data are means ± SD ( n = 3), ∗ P < 0.05.
Nadph Oxidase 2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "Downregulated Expression of Solute Carrier Family 26 Member 6 in NRK-52E Cells Attenuates Oxalate-Induced Intracellular Oxidative Stress"

Article Title: Downregulated Expression of Solute Carrier Family 26 Member 6 in NRK-52E Cells Attenuates Oxalate-Induced Intracellular Oxidative Stress

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2018/1724648

Higher Slc26a6 expression induced more intracellular ROS generation by oxalate. (a) Four cell types were stimulated with oxalate (700 μ M) for 3 h, and intracellular ROS levels were determined by fluorescence intensity of DCFH analyzed using flow cytometry. Changes before and after oxalate treatment are shown on the right graph as means ± SD ( n = 3). ∗ P < 0.05. (b) Lipid peroxidation was assessed by detecting the MDA level in supernatants of NRK cell lysates. NRK-Slc26a6 cells showed an obvious increase in MDA generation compared with control groups after oxalate treatment ( n = 6). (c) Activity change of superoxide dismutase (SOD) expressed as means ± SD. In the NRK-Slc26a6 group, SOD activity was markedly decreased compared to that in control groups. (d, e, f) Expressions of NADPH oxidase 2 (Nox2) and Nox4 before and after oxalate treatment in all groups using Western blot analysis. After oxalate treatment (700 μ M) for 24 h, the expression of Nox4 increased in the NRK-Slc26a6 group and that of Nox2 was decreased in the NRK-siRNA group. Data are means ± SD ( n = 3), ∗ P < 0.05.
Figure Legend Snippet: Higher Slc26a6 expression induced more intracellular ROS generation by oxalate. (a) Four cell types were stimulated with oxalate (700 μ M) for 3 h, and intracellular ROS levels were determined by fluorescence intensity of DCFH analyzed using flow cytometry. Changes before and after oxalate treatment are shown on the right graph as means ± SD ( n = 3). ∗ P < 0.05. (b) Lipid peroxidation was assessed by detecting the MDA level in supernatants of NRK cell lysates. NRK-Slc26a6 cells showed an obvious increase in MDA generation compared with control groups after oxalate treatment ( n = 6). (c) Activity change of superoxide dismutase (SOD) expressed as means ± SD. In the NRK-Slc26a6 group, SOD activity was markedly decreased compared to that in control groups. (d, e, f) Expressions of NADPH oxidase 2 (Nox2) and Nox4 before and after oxalate treatment in all groups using Western blot analysis. After oxalate treatment (700 μ M) for 24 h, the expression of Nox4 increased in the NRK-Slc26a6 group and that of Nox2 was decreased in the NRK-siRNA group. Data are means ± SD ( n = 3), ∗ P < 0.05.

Techniques Used: Expressing, Fluorescence, Flow Cytometry, Activity Assay, Western Blot


Structured Review

Proteintech nox2
Primers for real-time quantitative PCR analysis in humans.
Nox2, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nox2/product/Proteintech
Average 94 stars, based on 1 article reviews
Price from $9.99 to $1999.99
nox2 - by Bioz Stars, 2024-07
94/100 stars

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1) Product Images from "BCL6 Attenuates Proliferation and Oxidative Stress of Vascular Smooth Muscle Cells in Hypertension"

Article Title: BCL6 Attenuates Proliferation and Oxidative Stress of Vascular Smooth Muscle Cells in Hypertension

Journal: Oxidative Medicine and Cellular Longevity

doi: 10.1155/2019/5018410

Primers for real-time quantitative PCR analysis in humans.
Figure Legend Snippet: Primers for real-time quantitative PCR analysis in humans.

Techniques Used: Real-time Polymerase Chain Reaction, Sequencing

Primers for real-time quantitative PCR analysis in rats.
Figure Legend Snippet: Primers for real-time quantitative PCR analysis in rats.

Techniques Used: Real-time Polymerase Chain Reaction, Sequencing

Effects of BCL6 overexpression (OE) on Ang II-induced oxidative stress in VSMCs. The VSMCs were treated with empty plasmid or BCL6 plasmid (1 μ g/mL) for 24 h followed by PBS or Ang II (100 nM) treatment for 48 h. (a) NOX2 and NOX4 mRNA levels. (b) NOX2 and NOX4 protein expressions. (c) NAD(P)H oxidase activity. (d) ROS detected by dihydroethidium (DHE) staining. (e) Bar graph showing the relative fluorescence intensity of DHE. Values are mean ± SE. ∗ P < 0.05 vs. PBS; † P < 0.05 vs. Ctrl. n = 4 in (a) and (b); n = 6 in (c) and (d).
Figure Legend Snippet: Effects of BCL6 overexpression (OE) on Ang II-induced oxidative stress in VSMCs. The VSMCs were treated with empty plasmid or BCL6 plasmid (1 μ g/mL) for 24 h followed by PBS or Ang II (100 nM) treatment for 48 h. (a) NOX2 and NOX4 mRNA levels. (b) NOX2 and NOX4 protein expressions. (c) NAD(P)H oxidase activity. (d) ROS detected by dihydroethidium (DHE) staining. (e) Bar graph showing the relative fluorescence intensity of DHE. Values are mean ± SE. ∗ P < 0.05 vs. PBS; † P < 0.05 vs. Ctrl. n = 4 in (a) and (b); n = 6 in (c) and (d).

Techniques Used: Over Expression, Plasmid Preparation, Activity Assay, Staining, Fluorescence

Effects of BCL6 knockdown on Ang II-induced VSMC proliferation and oxidative stress in VSMCs. The cells were treated with Scr-shRNA or BCL6 shRNA (1 μ g/mL) for 24 h followed by treatment with PBS or Ang II (100 nM) for 48 h. (a) VSMC proliferation determined by CCK-8 assay. (b) PCNA protein expression. (c) NOX2 and NOX4 protein expressions. (d) ROS detected by dihydroethidium (DHE) staining. (e) Bar graph showing the relative fluorescence intensity of DHE. (f) BCL6 protein expression. Values are mean ± SE. ∗ P < 0.05 vs. PBS; † P < 0.05 vs. Ctrl. n = 6 for each group.
Figure Legend Snippet: Effects of BCL6 knockdown on Ang II-induced VSMC proliferation and oxidative stress in VSMCs. The cells were treated with Scr-shRNA or BCL6 shRNA (1 μ g/mL) for 24 h followed by treatment with PBS or Ang II (100 nM) for 48 h. (a) VSMC proliferation determined by CCK-8 assay. (b) PCNA protein expression. (c) NOX2 and NOX4 protein expressions. (d) ROS detected by dihydroethidium (DHE) staining. (e) Bar graph showing the relative fluorescence intensity of DHE. (f) BCL6 protein expression. Values are mean ± SE. ∗ P < 0.05 vs. PBS; † P < 0.05 vs. Ctrl. n = 6 for each group.

Techniques Used: shRNA, CCK-8 Assay, Expressing, Staining, Fluorescence

Effects of BCL6 overexpression (OE) on oxidative stress in the aortic media of WKY and SHR. (a) NOX2 and NOX4 mRNA levels. (b) NOX2 and NOX4 protein expressions. (c) ROS detected by dihydroethidium (DHE) staining in aorta. (d) Bar graph showing the relative fluorescence intensity of DHE. Values are mean ± SE. ∗ P < 0.05 vs. WKY; † P < 0.05 vs. Ctrl. n = 6 for each group.
Figure Legend Snippet: Effects of BCL6 overexpression (OE) on oxidative stress in the aortic media of WKY and SHR. (a) NOX2 and NOX4 mRNA levels. (b) NOX2 and NOX4 protein expressions. (c) ROS detected by dihydroethidium (DHE) staining in aorta. (d) Bar graph showing the relative fluorescence intensity of DHE. Values are mean ± SE. ∗ P < 0.05 vs. WKY; † P < 0.05 vs. Ctrl. n = 6 for each group.

Techniques Used: Over Expression, Staining, Fluorescence

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    AUDA administration alleviated cardiac dysfunction and reduced apoptosis in db/db mice heart. (a) Representative immunoblots and quantitation of soluble epoxide hydrolase (sEH) expression, (b) +dp/dt max, (c) -dp/dt min, (d) left ventricular ejection fraction (LVEF), (e) left ventricular internal diameter end systole (LVID(s)), (f) left ventricular internal diameter end diastole (LVID(d)), and (g) E/A ratio. (h and i) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice treated with or without the sEH inhibitor AUDA. (j and k) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (l–o) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia in different groups. Data were expressed as mean ± SEM ( n = 8 mice per group). ∗ p < 0.05 vs. Con and # p < 0.05 vs. DM or HGHF. Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; MABSA: mannitol+ BSA; DHE: dihydroethidium; HGHF: high glucose and high fat.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation

    doi: 10.1155/2022/3773415

    Figure Lengend Snippet: AUDA administration alleviated cardiac dysfunction and reduced apoptosis in db/db mice heart. (a) Representative immunoblots and quantitation of soluble epoxide hydrolase (sEH) expression, (b) +dp/dt max, (c) -dp/dt min, (d) left ventricular ejection fraction (LVEF), (e) left ventricular internal diameter end systole (LVID(s)), (f) left ventricular internal diameter end diastole (LVID(d)), and (g) E/A ratio. (h and i) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice treated with or without the sEH inhibitor AUDA. (j and k) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (l–o) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia in different groups. Data were expressed as mean ± SEM ( n = 8 mice per group). ∗ p < 0.05 vs. Con and # p < 0.05 vs. DM or HGHF. Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; MABSA: mannitol+ BSA; DHE: dihydroethidium; HGHF: high glucose and high fat.

    Article Snippet: The following antibodies were used: Bax (BosterBio, Pleasanton, CA, USA), Bcl2 (Boster), caspase-3 (Proteintech, Rosemont, IL, USA), cleaved caspase-3 (Cell Signaling Technology (CST), Danvers, MA, USA), NOX2 (Proteintech), NOX4 (Proteintech), SOD1 (Proteintech), Beclin 1 (CST), Atg3 (Santa Cruz Biotechnology, Dallas, TX, USA), LC3II (CST), and β -actin (Santa Cruz Biotechnology).

    Techniques: Western Blot, Quantitation Assay, Expressing, TUNEL Assay, Staining

    Small interfering RNA of Nrf2 specifically reduced the protective effects of AUDA on cardiomyocytes autophagy and apoptosis. (a and b) Representative immunoblots and quantitation of protein expression of Beclin 1, Atg3, and LC3II in HGHF-stimulated cardiomyocytes in different groups. (c) LC3-II/ β -actin ratio with or without bafilomycin A1 treatment under HGHF culture conditions. (d and e) Representative images of fluorescent LC3 puncta and quantitation of cardiomyocytes with different treatments. (f and g) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (h and i) Representative images and quantitation of cardiomyocyte apoptosis via the Annexin-V/PI apoptotic assay. (j and k) Representative images and quantitation of cardiomyocyte ROS levels via DCFH-DA. Data were expressed as mean ± SEM (n ≥ 3 per group). ∗ p < 0.05 vs. si-Con+Con and # p < 0.05 vs. si-Nrf2+Con. HGHF: high glucose and high fat.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation

    doi: 10.1155/2022/3773415

    Figure Lengend Snippet: Small interfering RNA of Nrf2 specifically reduced the protective effects of AUDA on cardiomyocytes autophagy and apoptosis. (a and b) Representative immunoblots and quantitation of protein expression of Beclin 1, Atg3, and LC3II in HGHF-stimulated cardiomyocytes in different groups. (c) LC3-II/ β -actin ratio with or without bafilomycin A1 treatment under HGHF culture conditions. (d and e) Representative images of fluorescent LC3 puncta and quantitation of cardiomyocytes with different treatments. (f and g) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the HGHF-stimulated cardiomyocytes pretreated with or without AUDA. (h and i) Representative images and quantitation of cardiomyocyte apoptosis via the Annexin-V/PI apoptotic assay. (j and k) Representative images and quantitation of cardiomyocyte ROS levels via DCFH-DA. Data were expressed as mean ± SEM (n ≥ 3 per group). ∗ p < 0.05 vs. si-Con+Con and # p < 0.05 vs. si-Nrf2+Con. HGHF: high glucose and high fat.

    Article Snippet: The following antibodies were used: Bax (BosterBio, Pleasanton, CA, USA), Bcl2 (Boster), caspase-3 (Proteintech, Rosemont, IL, USA), cleaved caspase-3 (Cell Signaling Technology (CST), Danvers, MA, USA), NOX2 (Proteintech), NOX4 (Proteintech), SOD1 (Proteintech), Beclin 1 (CST), Atg3 (Santa Cruz Biotechnology, Dallas, TX, USA), LC3II (CST), and β -actin (Santa Cruz Biotechnology).

    Techniques: Small Interfering RNA, Western Blot, Quantitation Assay, Expressing

    Virus carrying code for Nrf2 shRNA specifically reduced the protective effects of AUDA on apoptosis in db/db mice heart. (a and b) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice from different groups. (c–f) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia from different groups. (g) Mechanism diagram of full text. Data were expressed as mean ± SEM (n = 8 per group). ∗ p < 0.05 vs. ScshRNA +Con, # p < 0.05 vs. Nrf2shRNA+Con, and & p < 0.05 vs. Nrf2shRNA+DM. ScshRNA: AAV-ScshRNA; Nrf2shRNA: AAV-Nrf2shRNA; Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; DHE: dihydroethidium.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Soluble Epoxide Hydrolase Inhibition Protected against Diabetic Cardiomyopathy through Inducing Autophagy and Reducing Apoptosis Relying on Nrf2 Upregulation and Transcription Activation

    doi: 10.1155/2022/3773415

    Figure Lengend Snippet: Virus carrying code for Nrf2 shRNA specifically reduced the protective effects of AUDA on apoptosis in db/db mice heart. (a and b) Representative immunoblots and quantitation of protein expression of cleaved caspase-3, Bax, Bcl-2, NOX4, NOX2, and SOD1 in the myocardia of mice from different groups. (c–f) Histological analysis and quantitation of DHE, TUNEL, and 3-NT staining in the myocardia from different groups. (g) Mechanism diagram of full text. Data were expressed as mean ± SEM (n = 8 per group). ∗ p < 0.05 vs. ScshRNA +Con, # p < 0.05 vs. Nrf2shRNA+Con, and & p < 0.05 vs. Nrf2shRNA+DM. ScshRNA: AAV-ScshRNA; Nrf2shRNA: AAV-Nrf2shRNA; Con: db/m+vehicle; AUDA: db/m+AUDA; DM: db/db+vehicle; DHE: dihydroethidium.

    Article Snippet: The following antibodies were used: Bax (BosterBio, Pleasanton, CA, USA), Bcl2 (Boster), caspase-3 (Proteintech, Rosemont, IL, USA), cleaved caspase-3 (Cell Signaling Technology (CST), Danvers, MA, USA), NOX2 (Proteintech), NOX4 (Proteintech), SOD1 (Proteintech), Beclin 1 (CST), Atg3 (Santa Cruz Biotechnology, Dallas, TX, USA), LC3II (CST), and β -actin (Santa Cruz Biotechnology).

    Techniques: shRNA, Western Blot, Quantitation Assay, Expressing, TUNEL Assay, Staining

    VEGFR-3 knockdown accelerates Ang II-induced cardiac fibrosis, oxidative stress, and inflammation in mice. VEGFR-3 f/f and Lyve-1 Cre VEGFR-3 f/− mice were infused with saline or Ang II (1000 ng/kg/min) for 14 days. (a) Cardiac Masson staining (left) and quantitative analysis of the fibrotic area (%) (right, n = 6). (b) qPCR analyses of myocardial collagen I and collagen III levels ( n = 6). (c) Cardiac α -SMA immunohistochemical staining (left) and quantitative analysis of the positive area (right, n = 6). (d) qPCR analyses of myocardial α -SMA levels ( n = 6). (e) Cardiac DHE fluorescence staining (left) and quantitative analysis of relative fluorescence intensity (right, n = 6). (f) qPCR analyses of myocardial NOX2 and NOX4 levels ( n = 6). (g) CD68 (red) and DAPI (blue) fluorescence staining of heart sections (left) and quantification of CD68 + macrophages (right, n = 6). (h) qPCR analyses of myocardial IL-1 β and IL-6 levels ( n = 6). (i) Immunoblot analysis of cardiac TGF- β 1, p-Smad2/3, Smad2/3, NOX2, NOX4, p-P65, and P65 levels (left) and quantification (right, n = 4). The data are presented as the mean ± SD; n represents the number of animals in each group. Statistical differences were determined by two-way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the VEGFR-3 f/f +saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the VEGFR-3 f/f +Ang II group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms

    doi: 10.1155/2022/5044046

    Figure Lengend Snippet: VEGFR-3 knockdown accelerates Ang II-induced cardiac fibrosis, oxidative stress, and inflammation in mice. VEGFR-3 f/f and Lyve-1 Cre VEGFR-3 f/− mice were infused with saline or Ang II (1000 ng/kg/min) for 14 days. (a) Cardiac Masson staining (left) and quantitative analysis of the fibrotic area (%) (right, n = 6). (b) qPCR analyses of myocardial collagen I and collagen III levels ( n = 6). (c) Cardiac α -SMA immunohistochemical staining (left) and quantitative analysis of the positive area (right, n = 6). (d) qPCR analyses of myocardial α -SMA levels ( n = 6). (e) Cardiac DHE fluorescence staining (left) and quantitative analysis of relative fluorescence intensity (right, n = 6). (f) qPCR analyses of myocardial NOX2 and NOX4 levels ( n = 6). (g) CD68 (red) and DAPI (blue) fluorescence staining of heart sections (left) and quantification of CD68 + macrophages (right, n = 6). (h) qPCR analyses of myocardial IL-1 β and IL-6 levels ( n = 6). (i) Immunoblot analysis of cardiac TGF- β 1, p-Smad2/3, Smad2/3, NOX2, NOX4, p-P65, and P65 levels (left) and quantification (right, n = 4). The data are presented as the mean ± SD; n represents the number of animals in each group. Statistical differences were determined by two-way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 versus the VEGFR-3 f/f +saline group; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus the VEGFR-3 f/f +Ang II group.

    Article Snippet: The following antibodies were used: anti-VEGF-C (22601-1-AP, Proteintech), anti-VEGFR-3 (ab273148, Abcam), anti-p-p38 (ARG51850, Arigo), anti-p38 (ARG55258, Arigo), anti-VE-cadherin (ab205336, Abcam), anti-p-ERK1/2 (4370, CST), anti-ERK1/2 (4695S, CST), anti-p-AKT (9271S, CST), anti-AKT (9272, CST), anticalcineurin A (CaNA) (2614, CST), anti-p-STAT3 (9145, CST), anti-STAT3 (9139, CST), anti-TGF- β 1 (3711, CST), anti-p-Smad2/3 (882S, CST), anti-Smad2/3 (8685, CST), anti-NOX2 (19013-1-AP, Proteintech), anti-NOX4 (14347-1-AP, Proteintech), anti-p-P65 (3033, CST), anti-P65 (4764, CST), anti- β 2i (13635, CST), anti- β 5i (ARG41022, Arigo) anti-MKP5 (374276, Santa), and anti-GAPDH (5174, CST).

    Techniques: Staining, Immunohistochemical staining, Fluorescence, Western Blot

    Treatment of LXA4 inhibits oxidative stress in corpus cavernous of DMED rats. ( a ) Representative Western blot results for the p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox in rats of all the three groups. ( b ) Expressions of p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox with β-actin as the loading control in all the three groups were presented through bar graphs. ( c ) MDA levels determined by the ELISA method in all the three groups. ( d ) SOD activities determined by the ELISA method in all the three groups. Data are expressed as mean ± s.e.m. ( n control = 10, n DMED = 11, and n DMED + LXA4 = 11). * P < 0.05 and *** P < 0.001 when comparing two groups. DMED: diabetes mellitus-induced erectile dysfunction; LXA4: Lipoxin A4; ELISA: enzyme-linked immunosorbent assay; SOD: superoxide dismutase; MDA: malondialdehyde; s.e.m.: standard error of the mean.

    Journal: Asian Journal of Andrology

    Article Title: Lipoxin A4 improves erectile dysfunction in rats with type I diabetes by inhibiting oxidative stress and corporal fibrosis

    doi: 10.4103/aja.aja_49_17

    Figure Lengend Snippet: Treatment of LXA4 inhibits oxidative stress in corpus cavernous of DMED rats. ( a ) Representative Western blot results for the p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox in rats of all the three groups. ( b ) Expressions of p22 phox , p47 phox , gp91 phox , p40 phox , and p67 phox with β-actin as the loading control in all the three groups were presented through bar graphs. ( c ) MDA levels determined by the ELISA method in all the three groups. ( d ) SOD activities determined by the ELISA method in all the three groups. Data are expressed as mean ± s.e.m. ( n control = 10, n DMED = 11, and n DMED + LXA4 = 11). * P < 0.05 and *** P < 0.001 when comparing two groups. DMED: diabetes mellitus-induced erectile dysfunction; LXA4: Lipoxin A4; ELISA: enzyme-linked immunosorbent assay; SOD: superoxide dismutase; MDA: malondialdehyde; s.e.m.: standard error of the mean.

    Article Snippet: Equal amounts of protein samples (30 μg per lane) were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred to polyvinylidene difluoride membranes, followed by blocking in Tris-buffered saline-Tween (TBST) with 5% bovine serum albumin (BSA) for 1 h. Then, membranes were incubated with primary antibodies against: eNOS (1:1000; ab5589, Abcam, Cambridge, MA, USA), p-eNOS (Ser1177; 1:1000; 9571; Cell Signaling Technology, Danvers, MA, USA), neuronal nitric oxide synthase (nNOS; 1:1000; ab76067; Abcam), p22 phox (1:500; sc-271968, Santa Cruz, Dallas, Texas, USA), p47 phox (1:1000; D154042, Sangon Biotech, Shanghai, China), gp91 phox (1:500, 19013-1-AP, Proteintech); p40 phox (1:500; D154073, Sangon Biotech), p67 phox (1:1000; 15551-1-AP, Proteintech), α-smooth muscle actin (α-SMA; 1:1000; ab5694; Abcam), Collagen I (1:500; PB0981, Boster, Wuhan, China), Collagen IV (1:500; 19797-1-AP, Proteintech), TGF-β1 (1:1000; ab92486, Abcam), Smad2/3 (1:1000; 8685, Cell Signaling Technology), p-Smad2/3 (1:1000; 8828, Cell Signaling Technology), CTGF (1:1000; 23936-1-AP, Proteintech), and β-actin (1:1000, 20536-1-AP, Proteintech).

    Techniques: Western Blot, Enzyme-linked Immunosorbent Assay

    Higher Slc26a6 expression induced more intracellular ROS generation by oxalate. (a) Four cell types were stimulated with oxalate (700 μ M) for 3 h, and intracellular ROS levels were determined by fluorescence intensity of DCFH analyzed using flow cytometry. Changes before and after oxalate treatment are shown on the right graph as means ± SD ( n = 3). ∗ P < 0.05. (b) Lipid peroxidation was assessed by detecting the MDA level in supernatants of NRK cell lysates. NRK-Slc26a6 cells showed an obvious increase in MDA generation compared with control groups after oxalate treatment ( n = 6). (c) Activity change of superoxide dismutase (SOD) expressed as means ± SD. In the NRK-Slc26a6 group, SOD activity was markedly decreased compared to that in control groups. (d, e, f) Expressions of NADPH oxidase 2 (Nox2) and Nox4 before and after oxalate treatment in all groups using Western blot analysis. After oxalate treatment (700 μ M) for 24 h, the expression of Nox4 increased in the NRK-Slc26a6 group and that of Nox2 was decreased in the NRK-siRNA group. Data are means ± SD ( n = 3), ∗ P < 0.05.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Downregulated Expression of Solute Carrier Family 26 Member 6 in NRK-52E Cells Attenuates Oxalate-Induced Intracellular Oxidative Stress

    doi: 10.1155/2018/1724648

    Figure Lengend Snippet: Higher Slc26a6 expression induced more intracellular ROS generation by oxalate. (a) Four cell types were stimulated with oxalate (700 μ M) for 3 h, and intracellular ROS levels were determined by fluorescence intensity of DCFH analyzed using flow cytometry. Changes before and after oxalate treatment are shown on the right graph as means ± SD ( n = 3). ∗ P < 0.05. (b) Lipid peroxidation was assessed by detecting the MDA level in supernatants of NRK cell lysates. NRK-Slc26a6 cells showed an obvious increase in MDA generation compared with control groups after oxalate treatment ( n = 6). (c) Activity change of superoxide dismutase (SOD) expressed as means ± SD. In the NRK-Slc26a6 group, SOD activity was markedly decreased compared to that in control groups. (d, e, f) Expressions of NADPH oxidase 2 (Nox2) and Nox4 before and after oxalate treatment in all groups using Western blot analysis. After oxalate treatment (700 μ M) for 24 h, the expression of Nox4 increased in the NRK-Slc26a6 group and that of Nox2 was decreased in the NRK-siRNA group. Data are means ± SD ( n = 3), ∗ P < 0.05.

    Article Snippet: The PVDF membranes were blocked with 5% bovine serum albumin (BSA) for 2 h and probed with primary antibodies against Slc26a6 (1 : 200, sc-26728, Santa Cruz Biotechnology, CA, USA), NADPH oxidase 2 (Nox2, 1 : 200, 19013-1-AP, Proteintech, Hubei, China), Nox4 (1 : 200, 14347-1-AP, Proteintech, Hubei, China), NF κ B p65 (1 : 500, GB11142, Servicebio, Hubei, China), NF κ B-p65 (phosphorylated [p]-Ser536, 1 : 500, 11014, Signalway Antibody Co., Ltd, MD, USA), I κ B α (1 : 500, GB13212-1, Servicebio, Hubei, China), I κ B α (p-Ser32/36, 1 : 500, 11152, Signalway Antibody Co., Ltd, MD, USA), and OPN (1 : 200, 22952-1-AP, Proteintech, Hubei, China) at 4°C overnight.

    Techniques: Expressing, Fluorescence, Flow Cytometry, Activity Assay, Western Blot