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primary antibodies against nrf2  (Boster Bio)


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    Boster Bio primary antibodies against nrf2
    Effect of NOB, LPS, and INT on oxidative stress ( A ) and <t>Nrf2</t> signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.
    Primary Antibodies Against Nrf2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/primary antibodies against nrf2/product/Boster Bio
    Average 94 stars, based on 4 article reviews
    primary antibodies against nrf2 - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "Nobiletin Attenuates Inflammation and Modulates Lipid Metabolism in an In Vitro Model of Intestinal Failure-Associated Liver Disease"

    Article Title: Nobiletin Attenuates Inflammation and Modulates Lipid Metabolism in an In Vitro Model of Intestinal Failure-Associated Liver Disease

    Journal: Pharmaceutics

    doi: 10.3390/pharmaceutics18010087

    Effect of NOB, LPS, and INT on oxidative stress ( A ) and Nrf2 signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.
    Figure Legend Snippet: Effect of NOB, LPS, and INT on oxidative stress ( A ) and Nrf2 signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.

    Techniques Used: Protein-Protein interactions, Staining, Control, Imaging



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    primary antibodies against nrf2  (Boster Bio)
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    Effect of NOB, LPS, and INT on oxidative stress ( A ) and <t>Nrf2</t> signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.
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    rabbit anti rat primary antibodies against nrf2  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc rabbit anti rat primary antibodies against nrf2
    Levels of ferroptosis-related proteins in rat wound tissues. A: Western blot bar plot of the proteins; B: Nuclear factor E2-related factor 2 protein expression level; C: Heme oxygenase-1 protein expression level; D: Glutathione peroxidase 4 protein expression level. a P < 0.05 vs control; b P < 0.05 vs model; c P < 0.05 vs fish scale collagen. GPX4: Glutathione peroxidase 4; HO-1: Heme oxygenase-1; <t>Nrf2:</t> Nuclear factor E2-related factor 2; FSC: Fish scale collagen; Lip-1: Liproxstatin-1.
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    primary antibodies against anti nrf2  (Cell Signaling Technology Inc)
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    Astragaloside IV treatment enhanced <t>Nrf2</t> nuclear translocation. ( A ) Western blot analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression in prostate tissues from EAP model and AS-IV-treated rats. ( B – E ) Quantitative analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression levels via Western blot. ( F – I ) Serum biomarkers analysis: Glutathione (GSH), superoxide dismutase (SOD), iron ion levels, and lactate dehydrogenase (LDH) activity. ( J and K ) Enhanced Nrf2 immunoreactivity demonstrated by immunohistochemical (IHC) and immunofluorescence (IF) staining in AS-IV-treated group. Data represent mean ± SD. Statistical significance determined by one-way ANOVA ( B – I ). Significance thresholds: ns (not significant) P >0.05; * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001.
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    Image Search Results


    Schematic illustration of the synthesis and therapeutic mechanism of mitochondria‐targeted T‐Ag SA ‐CDs for AKI therapy. In cisplatin‐induced AKI, T‐Ag SA ‐CDs (<10 nm) scavenge ROS via SOD‐ and GP X ‐like activities, restore mitochondrial membrane potential (Ψm), and activate the KEAP‐1/Nrf2 pathway, thereby upregulating HO‐1 and GPX4 to enhance antioxidant defense and alleviate renal injury.

    Journal: Advanced Science

    Article Title: Precision‐Engineered Silver Single‐Atom Carbon Dot Nanozymes for Theranostic Management of Acute Kidney Injury

    doi: 10.1002/advs.202519393

    Figure Lengend Snippet: Schematic illustration of the synthesis and therapeutic mechanism of mitochondria‐targeted T‐Ag SA ‐CDs for AKI therapy. In cisplatin‐induced AKI, T‐Ag SA ‐CDs (<10 nm) scavenge ROS via SOD‐ and GP X ‐like activities, restore mitochondrial membrane potential (Ψm), and activate the KEAP‐1/Nrf2 pathway, thereby upregulating HO‐1 and GPX4 to enhance antioxidant defense and alleviate renal injury.

    Article Snippet: Primary antibodies against NRF2 (80593‐1‐RR), KEAP1 (80744‐1‐RR), HO‐1 (81281‐1‐RR), GPX4 (82822‐2‐RR), β‐actin (81115‐1‐RR), and NF‐κB (80979‐1‐RR), and HRP‐conjugated goat anti‐rabbit IgG secondary antibody (SA00001‐2), were obtained from Proteintech Group, Inc. Chemiluminescent detection was performed using the SuperKine West Pico PLUS substrate (BMU101‐CN, Abbkine Scientific Co., Ltd.).

    Techniques: Membrane

    Molecular and cellular responses to CDs based AKI response. a) Schematic representation of the cellular pathway involving KEAP1, NRF2, and downstream targets (HO‐1, GPX4) in response to AKI. b) Western blot analysis showing protein expression levels of KEAP1, NRF2, GPX4, HO‐1, and NF‐κB across experimental conditions (I: H 2 O 2 ; II: H 2 O 2 + N‐CDs; III: H 2 O 2 + Ag SA ‐CDs; IV: H 2 O 2 + T‐Ag SA ‐CDs and V: PBS) against β‐actin as a loading control. c) Ex vivo fluorescence imaging of N‐CDs, Ag SA ‐CDs, and T‐Ag SA ‐CDs at 1, 3, 6, 12, and 24 h, indicating time‐dependent changes in uptake and fluorescence intensity. d) Ex vivo biodistribution data of CDs in brain, heart, lung, spleen, liver, and kidney at 1, 2, 3, 6, 12, and 24 h, visualized through fluorescence imaging with a color scale representing signal intensity. e) Quantitative analysis of T‐Ag SA ‐CDs accumulation (% ID/g) in major organs (kidney, liver, lung, heart, brain, and spleen) time points of post‐injection ( n = 3 biologically independent mice). The i.v. dosage: 200 µL. Error bars represent standard deviations ( n = 3).

    Journal: Advanced Science

    Article Title: Precision‐Engineered Silver Single‐Atom Carbon Dot Nanozymes for Theranostic Management of Acute Kidney Injury

    doi: 10.1002/advs.202519393

    Figure Lengend Snippet: Molecular and cellular responses to CDs based AKI response. a) Schematic representation of the cellular pathway involving KEAP1, NRF2, and downstream targets (HO‐1, GPX4) in response to AKI. b) Western blot analysis showing protein expression levels of KEAP1, NRF2, GPX4, HO‐1, and NF‐κB across experimental conditions (I: H 2 O 2 ; II: H 2 O 2 + N‐CDs; III: H 2 O 2 + Ag SA ‐CDs; IV: H 2 O 2 + T‐Ag SA ‐CDs and V: PBS) against β‐actin as a loading control. c) Ex vivo fluorescence imaging of N‐CDs, Ag SA ‐CDs, and T‐Ag SA ‐CDs at 1, 3, 6, 12, and 24 h, indicating time‐dependent changes in uptake and fluorescence intensity. d) Ex vivo biodistribution data of CDs in brain, heart, lung, spleen, liver, and kidney at 1, 2, 3, 6, 12, and 24 h, visualized through fluorescence imaging with a color scale representing signal intensity. e) Quantitative analysis of T‐Ag SA ‐CDs accumulation (% ID/g) in major organs (kidney, liver, lung, heart, brain, and spleen) time points of post‐injection ( n = 3 biologically independent mice). The i.v. dosage: 200 µL. Error bars represent standard deviations ( n = 3).

    Article Snippet: Primary antibodies against NRF2 (80593‐1‐RR), KEAP1 (80744‐1‐RR), HO‐1 (81281‐1‐RR), GPX4 (82822‐2‐RR), β‐actin (81115‐1‐RR), and NF‐κB (80979‐1‐RR), and HRP‐conjugated goat anti‐rabbit IgG secondary antibody (SA00001‐2), were obtained from Proteintech Group, Inc. Chemiluminescent detection was performed using the SuperKine West Pico PLUS substrate (BMU101‐CN, Abbkine Scientific Co., Ltd.).

    Techniques: Western Blot, Expressing, Control, Ex Vivo, Fluorescence, Imaging, Injection

    Effect of NOB, LPS, and INT on oxidative stress ( A ) and Nrf2 signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.

    Journal: Pharmaceutics

    Article Title: Nobiletin Attenuates Inflammation and Modulates Lipid Metabolism in an In Vitro Model of Intestinal Failure-Associated Liver Disease

    doi: 10.3390/pharmaceutics18010087

    Figure Lengend Snippet: Effect of NOB, LPS, and INT on oxidative stress ( A ) and Nrf2 signaling pathways ( B ). ROS levels in THLE-2 cells after 24 h treatment with LPS, INT, INT+LPS, and INT+LPS+NOB (25 µM). Non-treated cells and DOXO (100 nM) served as negative and positive controls, respectively. ROS (+) and ROS (−) indicate cells with detectable or undetectable superoxide radicals, respectively. Representative histograms are shown, and data represent mean ± SEM from two independent experiments run in duplicate. Nrf2 subcellular distribution (cytosolic and nuclear fractions) and cytosolic SOD1 levels in THLE-2 cells after 24 h treatment. Representative blots are shown along with the corresponding Stain-Free™ total protein images used for total protein normalization (TPN). Lane order: (1) control, (2) LPS, (3) INT, (4) INT+LPS, (5) INT+LPS+NOB (10 µM), (6) INT+LPS+NOB (25 µM). Band intensities were quantified by densitometry and normalized to the lane-specific total protein signal obtained from Stain-Free imaging. Data are presented as mean ± SEM from two independent experiments, each performed in duplicate. Asterisks above denotes statistical significance relative to the untreated control cells with * p < 0.05, ** p < 0.01. Hashtags above denotes statistical significance relative to the INT+LPS-treated cells with # p < 0.05, ## p < 0.01, ### p < 0.001.

    Article Snippet: Target proteins were detected using primary antibodies against Nrf2 and SOD1 (Santa Cruz Biotechnology, Dallas, TX, USA), followed by AP- or HRP-conjugated secondary antibodies (Santa Cruz Biotechnology, Dallas, TX, USA and BosterBio, Pleasanton, CA, USA).

    Techniques: Protein-Protein interactions, Staining, Control, Imaging

    Levels of ferroptosis-related proteins in rat wound tissues. A: Western blot bar plot of the proteins; B: Nuclear factor E2-related factor 2 protein expression level; C: Heme oxygenase-1 protein expression level; D: Glutathione peroxidase 4 protein expression level. a P < 0.05 vs control; b P < 0.05 vs model; c P < 0.05 vs fish scale collagen. GPX4: Glutathione peroxidase 4; HO-1: Heme oxygenase-1; Nrf2: Nuclear factor E2-related factor 2; FSC: Fish scale collagen; Lip-1: Liproxstatin-1.

    Journal: World Journal of Diabetes

    Article Title: Effect of fish scale ointment on diabetic foot ulcer by inducing ferroptosis via the nuclear factor E2-related factor 2 pathway

    doi: 10.4239/wjd.v16.i12.111789

    Figure Lengend Snippet: Levels of ferroptosis-related proteins in rat wound tissues. A: Western blot bar plot of the proteins; B: Nuclear factor E2-related factor 2 protein expression level; C: Heme oxygenase-1 protein expression level; D: Glutathione peroxidase 4 protein expression level. a P < 0.05 vs control; b P < 0.05 vs model; c P < 0.05 vs fish scale collagen. GPX4: Glutathione peroxidase 4; HO-1: Heme oxygenase-1; Nrf2: Nuclear factor E2-related factor 2; FSC: Fish scale collagen; Lip-1: Liproxstatin-1.

    Article Snippet: Membranes were then incubated overnight at 4 °C with rabbit anti-rat primary antibodies against Nrf2 (No. 12721, 1:1000), heme oxygenase-1 (HO-1) (No. 70081, 1:1000), glutathione peroxidase 4 (GPX4; No. 52455, 1:1000), and β-actin (No. 4967, 1:1000), all from Cell Signaling Technology, United States.

    Techniques: Western Blot, Expressing, Control

    Astragaloside IV treatment enhanced Nrf2 nuclear translocation. ( A ) Western blot analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression in prostate tissues from EAP model and AS-IV-treated rats. ( B – E ) Quantitative analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression levels via Western blot. ( F – I ) Serum biomarkers analysis: Glutathione (GSH), superoxide dismutase (SOD), iron ion levels, and lactate dehydrogenase (LDH) activity. ( J and K ) Enhanced Nrf2 immunoreactivity demonstrated by immunohistochemical (IHC) and immunofluorescence (IF) staining in AS-IV-treated group. Data represent mean ± SD. Statistical significance determined by one-way ANOVA ( B – I ). Significance thresholds: ns (not significant) P >0.05; * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001.

    Journal: Journal of Inflammation Research

    Article Title: Astragaloside IV Attenuates Chronic Prostatitis by Activating Keap1/Nrf2/HO-1 Pathway: Suppressing Ferroptosis and Enhancing Antioxidant Defense

    doi: 10.2147/JIR.S527722

    Figure Lengend Snippet: Astragaloside IV treatment enhanced Nrf2 nuclear translocation. ( A ) Western blot analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression in prostate tissues from EAP model and AS-IV-treated rats. ( B – E ) Quantitative analysis of GPX4, Keap1, Nrf2, and HO-1 protein expression levels via Western blot. ( F – I ) Serum biomarkers analysis: Glutathione (GSH), superoxide dismutase (SOD), iron ion levels, and lactate dehydrogenase (LDH) activity. ( J and K ) Enhanced Nrf2 immunoreactivity demonstrated by immunohistochemical (IHC) and immunofluorescence (IF) staining in AS-IV-treated group. Data represent mean ± SD. Statistical significance determined by one-way ANOVA ( B – I ). Significance thresholds: ns (not significant) P >0.05; * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001.

    Article Snippet: Primary antibodies against Anti-Nrf2 (#12721), Anti-Keap1 (#8047), Anti-xCT (#98051), Anti-GPX4 (#52455), Anti-GAPDH (#2118), and Anti-β-actin (#4970) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Translocation Assay, Western Blot, Expressing, Activity Assay, Immunohistochemical staining, Immunofluorescence, Staining

    Molecular docking analysis of AS-IV with Keap1 and Nrf2. ( A ) Nrf2 (cyan) PHE-83, GLU-82, THR-80, GLU-79, GLU-78 and ASN-382, ARG-380, ARG-415, SER-555, TYR-525 on Keap1 (blue) could form five hydrogen bond interactions. ( B ) AS-IV could form five hydrogen bonds with LEU-84, ASP-77, GLU-78 and GLU-79 on Nrf2, and one hydrogen bond with ARG-415 on Keap1.

    Journal: Journal of Inflammation Research

    Article Title: Astragaloside IV Attenuates Chronic Prostatitis by Activating Keap1/Nrf2/HO-1 Pathway: Suppressing Ferroptosis and Enhancing Antioxidant Defense

    doi: 10.2147/JIR.S527722

    Figure Lengend Snippet: Molecular docking analysis of AS-IV with Keap1 and Nrf2. ( A ) Nrf2 (cyan) PHE-83, GLU-82, THR-80, GLU-79, GLU-78 and ASN-382, ARG-380, ARG-415, SER-555, TYR-525 on Keap1 (blue) could form five hydrogen bond interactions. ( B ) AS-IV could form five hydrogen bonds with LEU-84, ASP-77, GLU-78 and GLU-79 on Nrf2, and one hydrogen bond with ARG-415 on Keap1.

    Article Snippet: Primary antibodies against Anti-Nrf2 (#12721), Anti-Keap1 (#8047), Anti-xCT (#98051), Anti-GPX4 (#52455), Anti-GAPDH (#2118), and Anti-β-actin (#4970) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques:

    Therapeutic mechanism of Astragaloside IV in experimental autoimmune prostatitis. AS-IV ameliorates chronic prostatitis/chronic pelvic pain syndrome in EAP rats through three core mechanisms:1. Keap1/Nrf2/HO-1 axis activation; 2. Iron homeostasis regulation; 3. Oxidative damage suppression.

    Journal: Journal of Inflammation Research

    Article Title: Astragaloside IV Attenuates Chronic Prostatitis by Activating Keap1/Nrf2/HO-1 Pathway: Suppressing Ferroptosis and Enhancing Antioxidant Defense

    doi: 10.2147/JIR.S527722

    Figure Lengend Snippet: Therapeutic mechanism of Astragaloside IV in experimental autoimmune prostatitis. AS-IV ameliorates chronic prostatitis/chronic pelvic pain syndrome in EAP rats through three core mechanisms:1. Keap1/Nrf2/HO-1 axis activation; 2. Iron homeostasis regulation; 3. Oxidative damage suppression.

    Article Snippet: Primary antibodies against Anti-Nrf2 (#12721), Anti-Keap1 (#8047), Anti-xCT (#98051), Anti-GPX4 (#52455), Anti-GAPDH (#2118), and Anti-β-actin (#4970) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Activation Assay