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rabbit polyclonal anti nrf2  (Proteintech)


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    Proteintech rabbit polyclonal anti nrf2
    Rabbit Polyclonal Anti Nrf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2086 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+nrf2/NRF2%2C+NFE2L2+Antibody/pmc13011206-161-29-34
    Average 96 stars, based on 2086 article reviews
    rabbit polyclonal anti nrf2 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: Study on the potential mechanism of Artemisia integrifolia Linn. in diabetic nephropathy: multiscale analysis of network pharmacology and metabolomics.
    Article Snippet: Ethnopharmacological relevance: Artemisia integrifolia Linn. (Chinese name: Liuhao, LH) is a traditional Chinese medicine commonly employed for managing diabetes.. However, its pharmacological effects on diabetic nephropathy (DN) remain unclear.. Aim of the study: This study aimed to investigate the effects and underlying mechanisms of LH on DN.

    Incubation:

    Article Title: Study on the potential mechanism of Artemisia integrifolia Linn. in diabetic nephropathy: multiscale analysis of network pharmacology and metabolomics.
    Article Snippet: Ethnopharmacological relevance: Artemisia integrifolia Linn. (Chinese name: Liuhao, LH) is a traditional Chinese medicine commonly employed for managing diabetes.. However, its pharmacological effects on diabetic nephropathy (DN) remain unclear.. Aim of the study: This study aimed to investigate the effects and underlying mechanisms of LH on DN.

    Article Title: Aspergillus oryzae solid-state fermentation enriches protopanaxatriol-type ginsenosides in Panax ginseng and confers cytoprotective effects in vitro
    Article Snippet: Equal amounts of protein (20 μg per lane) were separated by 10% SDS-PAGE and transferred onto PVDF membranes (Beyotime, FFP39) using a wet transfer system at a constant current of 120 mA for 120 min. .. The membranes were blocked with 5% non-fat milk for 2 h at room temperature and then incubated overnight at 4 °C with the following primary antibodies diluted in 5% BSA: anti-Bax (Proteintech, 50599-2-lg; 1:1,000), anti-Bcl-2 (Proteintech, 68103-1-lg; 1:1,000), anti-Nrf2 (Proteintech, 16396-1-AP; 1:1,000), and anti-β-actin (Mouse monoclonal, Proteintech, 60008-1-lg; 1:5,000). .. After washing three times with TBST, the membranes were incubated with HRP-conjugated goat anti-rabbit (Proteintech, RGAR001; 1:10,000) and goat anti-mouse (Proteintech, RGAM011; 1:10,000) secondary antibodies for 2 h at room temperature.

    Western Blot:

    Article Title: Indole-3-carbinol attenuates cisplatin-induced premature ovarian failure by activating Nrf2 through competitive binding of Keap1.
    Article Snippet: Background: Premature ovarian failure (POF) leads to female infertility and significantly increases long-term health risks.. However, available drugs that can reverse this condition are lacking.. Purpose: To elucidate the role of nuclear factor erythroid 2-related factor (Nrf2) in POF and the underlying molecular mechanism through which indole-3-carbinol (I3C) alleviates POF.

    other:

    Article Title: NRF2-TERT-ACSL4 pathway inhibits ferroptosis and regulates cytoskeletal dynamics to mitigate ovarian aging.
    Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.



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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
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    Combination therapy enhances endothelial integrity and activates <t>NRF2/HO‐1</t> and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.
    Rabbit Polyclonal Anti Nrf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 <t>(NRF2).</t> β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.
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    BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 <t>(NRF2).</t> β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.
    Anti Nrf2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proteintech anti nrf2
    BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 <t>(NRF2).</t> β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.
    Anti Nrf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Combination therapy enhances endothelial integrity and activates NRF2/HO‐1 and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.

    Journal: Journal of Diabetes Investigation

    Article Title: Liraglutide combined with dapagliflozin treatment improves myocardial disease and endothelial dysfunction in T2DM mice

    doi: 10.1111/jdi.70363

    Figure Lengend Snippet: Combination therapy enhances endothelial integrity and activates NRF2/HO‐1 and AMPK/PKA‐eNOS pathways to counteract vascular oxidative stress. (a) Immunofluorescence staining of aortic sections for CD31 (endothelial marker, red) and 3‐nitrotyrosine (3‐NT, oxidative damage marker, green); nuclei stained with DAPI (blue). Scale bar: 50 μm. (b) Quantification of CD31 + area (%) and 3‐NT fluorescence intensity ( n = 6 per group). (c) Western blot analysis of NRF2, HO‐1, phospho‐AMPK (Thr172), total AMPK, PKA substrate phosphorylation, eNOS, and phospho‐eNOS (Ser1177) in aortic tissue. β‐Actin served as loading control, n = 3. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01 vs. control; ## P < 0.01 vs. model.

    Article Snippet: Membranes were blocked with 5% (w/v) non‐fat milk (A600669‐0250, Sangon Biotech) in TBST for 1.5 h at room temperature and then incubated overnight at 4°C with the following primary antibodies at specified dilutions: TNF‐α (1:1,000, 17590‐1‐AP, Proteintech), IL‐1β (1:1,000, AF5103, Affinity), IL‐6 (1:500, GB11117, Servicebio), Bax (1:8,000, 50599‐2‐Ig, Proteintech), BCl‐2 (1:1,000, AF6139, Affinity), cleaved caspase‐3 (1:1,000, AF7022, Affinity), 3‐NT (1:1,000, HY‐ P81216 , MCE), NRF2 (1:1,000, BF8017, Affinity), HO‐1 (1:20,000, 10,701‐1‐AP, Proteintech), p‐AMPK (1:1,000, AF3423, Affinity), AMPK (1:1,000, AF6423, Affinity), PKA (1:1,000, AF7746, Affinity), p‐eNOS (1:1,000, AF3247, Affinity), and eNOS (1:20,000, 27120‐1‐AP, Proteintech).

    Techniques: Immunofluorescence, Staining, Marker, Fluorescence, Western Blot, Phospho-proteomics, Control

    BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 (NRF2). β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.

    Journal: Current Therapeutic Research, Clinical and Experimental

    Article Title: The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury

    doi: 10.1016/j.curtheres.2026.100825

    Figure Lengend Snippet: BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 (NRF2). β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.

    Article Snippet: Antibodies against GPX4 (Catalog #3F5G5), HO-1 (Catalog #10701-1-AP), NRF2 (Catalog #16396-1-AP), VDAC (Catalog #10866-1-AP), Cleaved Caspase-3 (Catalog #68773-1-Ig), and CD45 (Catalog #98035-1-RR) were purchased from Proteintech.

    Techniques: Fluorescence, Colorimetric Assay, Immunofluorescence, Western Blot, Control