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antibody against nrf 2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibody against nrf 2
    Antibody Against Nrf 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibody against nrf 2/product/Cell Signaling Technology Inc
    Average 93 stars, based on 42 article reviews
    antibody against nrf 2 - by Bioz Stars, 2026-02
    93/100 stars

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    Preparation of RCDs/UA@Lipo-HAMA and schematic diagram of therapeutic mechanisms against adhesion. ( A ) Preparation of RCDs/UA@Lipo for dual-drug co-loading. ( B ) The mixture of RCDs/UA@Lipo and HAMA was precisely applied to the periphery of the sutured tendon model and photocured using 365 nm UV irradiation. This process solidified the HAMA, enabling a localized and sustained release of RCDs and UA. ( C ) RCDs/UA@Lipo-HAMA diminishes oxidative stress by activating <t>Nrf2/HO-1,</t> reducing CD68, and iNOS, and suppressing fibrosis proteins, thereby lessening inflammation and fibrosis, reducing tendon adhesion, and promoting healing.
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    Image Search Results


    Immunohistochemical detection of Nrf2 expression (x 400). ( A , B ) Control and vilda alone groups showed minimal immunostaining, respectively. ( C ) Ovaries from irradiated rats showed extensive brown immunostaining (increased cytoplasmic Nrf2). ( D ) Vilda co-administration resulted in a marked reduction in cytoplasmic Nrf2. ( E ) Quantitative image analysis for Nrf2 immunostaining was expressed as optical density (O.D.). ( F ) Scoring of the immunostaining considering both the staining intensity and the percentage of positive cells

    Journal: BMC Pharmacology & Toxicology

    Article Title: Can vildagliptin protect against radiation-induced premature ovarian failure? Insights into the AMPK and AKT signaling pathways

    doi: 10.1186/s40360-025-00903-5

    Figure Lengend Snippet: Immunohistochemical detection of Nrf2 expression (x 400). ( A , B ) Control and vilda alone groups showed minimal immunostaining, respectively. ( C ) Ovaries from irradiated rats showed extensive brown immunostaining (increased cytoplasmic Nrf2). ( D ) Vilda co-administration resulted in a marked reduction in cytoplasmic Nrf2. ( E ) Quantitative image analysis for Nrf2 immunostaining was expressed as optical density (O.D.). ( F ) Scoring of the immunostaining considering both the staining intensity and the percentage of positive cells

    Article Snippet: The slides were then blocked with 5% bovine serum albumin in tris-buffered saline for 2 h. The sections were then immunostained with Nrf2 primary antibody: rabbit polyclonal anti-rat Nrf2 antibody (ABclonal, Cat No. A0674) at a concentration of 1 μg/ml containing 5% bovine serum albumin in tris-buffered saline and incubated overnight at 4 °C.

    Techniques: Immunohistochemical staining, Expressing, Control, Immunostaining, Irradiation, Staining

    CHRE suppressed oxidative stress in the hippocampus of Aβ1−42 ‑induced rats. The alteration of ( A ) SOD, ( B ) CAT, ( C ) GPx enzyme activities, and ( D ) MDA levels were investigated by oxidative stress assays. ( E ) Quantitative analysis of Nrf2 protein expression, and ( F ) cropped immunoblots in the hippocampus were determined by Western blotting ( n = 8, each group). Original blots were presented in Supplementary Fig. . Data were expressed as mean ± SD. ### P < 0.001 compared with SC group; *** P < 0.001, ** P < 0.01 compared with V + Aβ group. Aβ: amyloid-β; CAT: catalase; CHRE: Clausena harmandiana root extract; GAPDH: glyceraldehyde 3 phosphate dehydrogenase; GPx: glutathione peroxidase; MDA: malondialdehyde; Nrf2: nuclear factor erythroid 2-related factor 2; SC: sham control; SOD: superoxide dismutase; V: vehicle; Vit C: vitamin C

    Journal: BMC Complementary Medicine and Therapies

    Article Title: Clausena harmandiana root extract ameliorates Aβ 1-42 induced cognitive deficits, oxidative stress, and apoptosis in rats

    doi: 10.1186/s12906-024-04662-4

    Figure Lengend Snippet: CHRE suppressed oxidative stress in the hippocampus of Aβ1−42 ‑induced rats. The alteration of ( A ) SOD, ( B ) CAT, ( C ) GPx enzyme activities, and ( D ) MDA levels were investigated by oxidative stress assays. ( E ) Quantitative analysis of Nrf2 protein expression, and ( F ) cropped immunoblots in the hippocampus were determined by Western blotting ( n = 8, each group). Original blots were presented in Supplementary Fig. . Data were expressed as mean ± SD. ### P < 0.001 compared with SC group; *** P < 0.001, ** P < 0.01 compared with V + Aβ group. Aβ: amyloid-β; CAT: catalase; CHRE: Clausena harmandiana root extract; GAPDH: glyceraldehyde 3 phosphate dehydrogenase; GPx: glutathione peroxidase; MDA: malondialdehyde; Nrf2: nuclear factor erythroid 2-related factor 2; SC: sham control; SOD: superoxide dismutase; V: vehicle; Vit C: vitamin C

    Article Snippet: The protein membranes were blocked with 5% bovine serum albumin (BSA; Merck Millipore, Germany) diluted in 0.1% tris-buffer saline containing tween 20 (TBST) for 1 h. Subsequently, each membrane was individually probed with primary antibodies at 4 °C overnight including rat monoclonal anti-Nrf2 antibody (1:2,000 dilution; Merck Millipore Corporation, Billerica, USA) and rabbit polyclonal anti-caspase 3 antibody (1:4,000; Sigma-Aldrich, USA) diluted in 5% BSA in TBST, and mouse monoclonal anti-glyceraldehyde 3 phosphate dehydrogenase antibody (GAPDH, 1:20,000 dilution; Abcam, UK) diluted in 5% skim milk in TBST.

    Techniques: Expressing, Western Blot, Control

    Preparation of RCDs/UA@Lipo-HAMA and schematic diagram of therapeutic mechanisms against adhesion. ( A ) Preparation of RCDs/UA@Lipo for dual-drug co-loading. ( B ) The mixture of RCDs/UA@Lipo and HAMA was precisely applied to the periphery of the sutured tendon model and photocured using 365 nm UV irradiation. This process solidified the HAMA, enabling a localized and sustained release of RCDs and UA. ( C ) RCDs/UA@Lipo-HAMA diminishes oxidative stress by activating Nrf2/HO-1, reducing CD68, and iNOS, and suppressing fibrosis proteins, thereby lessening inflammation and fibrosis, reducing tendon adhesion, and promoting healing.

    Journal: International Journal of Nanomedicine

    Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

    doi: 10.2147/IJN.S466312

    Figure Lengend Snippet: Preparation of RCDs/UA@Lipo-HAMA and schematic diagram of therapeutic mechanisms against adhesion. ( A ) Preparation of RCDs/UA@Lipo for dual-drug co-loading. ( B ) The mixture of RCDs/UA@Lipo and HAMA was precisely applied to the periphery of the sutured tendon model and photocured using 365 nm UV irradiation. This process solidified the HAMA, enabling a localized and sustained release of RCDs and UA. ( C ) RCDs/UA@Lipo-HAMA diminishes oxidative stress by activating Nrf2/HO-1, reducing CD68, and iNOS, and suppressing fibrosis proteins, thereby lessening inflammation and fibrosis, reducing tendon adhesion, and promoting healing.

    Article Snippet: After permeabilized and blocked, the sections were incubated with rabbit anti-rat antibodies against Nrf2 (1:200; Cat# 80593-1-RR, Proteintech, USA), HO-1 (1:200; Cat#10701-1-AP, Proteintech, USA), CD68 (1:300; GB11067, Servicebio, China), and iNOS (1:200; Cat#18985-1-AP, Proteintech, USA) at 4°C overnight.

    Techniques: Irradiation