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antibodies against nrf2  (MedChemExpress)
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MedChemExpress antibodies against nrf2
Antibodies Against Nrf2, supplied by MedChemExpress, 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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primary antibodies against nrf2  (Proteintech)
96
Proteintech primary antibodies against nrf2
CT alleviates UVA-induced ER stress and apoptosis via <t>Nrf2</t> in HaCaT cells. (A) HaCaT cells were subjected to UVA radiation and treated with 50 or 100 μg/mL CT and/or siNrf2. Western blot assays were performed to detect the levels of ATF6, phosphorylated elF2a (p-elF2a), CHOP, GADD34, Cleaved caspase9, Cleaved caspase3, JNK, phosphorylated JNK (p-JNK), Bax, BCL2, cytoplasmic and nuclear NRF2 and HO-1. (B) Flow cytometry analysis was performed to determine cell apoptosis. Quantification of the percentage of apoptotic cells in different treatments. (C) Heatmap generated the data from RNAseq. Genes are all related to NRF2 downstream anti-oxidant or detoxification target genes. The figure was generated by SRplot . N = 4. * p ≤ 0.05; ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001.
Primary Antibodies Against 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
https://www.bioz.com/result/primary antibodies against nrf2/product/Proteintech
Average 96 stars, based on 1 article reviews
primary antibodies against nrf2 - by Bioz Stars, 2026-02
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antibodies against nrf2  (Proteintech)
96
Proteintech antibodies against nrf2
Cynarin suppresses macrophage-mediated inflammation through activation of the <t>Nrf2-Keap1</t> signalling pathway. (A) RAW264.7 cells were exposed to cynarin (10, 50 or 100 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of IL1β , IL6 , Nos2 and Tnf were detected by RT-qPCR (n=3). (B) RAW264.7 cells and bone marrow-derived macrophages were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Intracellular ROS levels were measured with a ROS assay kit (n=3). (C) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 6 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of Nrf2 , Keap1 , Hmox1 and Cat were detected by RT-qPCR (n=3). (D) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Expression levels of Nrf2, Keap1 and HO-1 were detected by WB. (E) RAW264.7 cells were exposed to 100 μ M cynarin for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Nuclear extracts and cytoplasmic extracts were used to test expression of Nrf2 by WB. (F) Quantitative densitometric analysis was performed to normalize Nrf2, Keap1 and HO-1 expression levels from D (n=3). (G) Quantitative densitometric analysis was performed to normalize Nrf2 expression levels from E (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001 vs. CTL and LPS group separately. LPS, lipopolysaccharide; RT-qPCR, reverse transcription-quantitative PCR; ROS, reactive oxygen species; HO-1, heme oxygenase-1; WB, western blotting.
Antibodies Against 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
https://www.bioz.com/result/antibodies against nrf2/product/Proteintech
Average 96 stars, based on 1 article reviews
antibodies against nrf2 - by Bioz Stars, 2026-02
96/100 stars
  Buy from Supplier
antibody against nrf2  (Proteintech)
96
Proteintech antibody against nrf2
Cynarin suppresses macrophage-mediated inflammation through activation of the <t>Nrf2-Keap1</t> signalling pathway. (A) RAW264.7 cells were exposed to cynarin (10, 50 or 100 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of IL1β , IL6 , Nos2 and Tnf were detected by RT-qPCR (n=3). (B) RAW264.7 cells and bone marrow-derived macrophages were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Intracellular ROS levels were measured with a ROS assay kit (n=3). (C) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 6 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of Nrf2 , Keap1 , Hmox1 and Cat were detected by RT-qPCR (n=3). (D) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Expression levels of Nrf2, Keap1 and HO-1 were detected by WB. (E) RAW264.7 cells were exposed to 100 μ M cynarin for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Nuclear extracts and cytoplasmic extracts were used to test expression of Nrf2 by WB. (F) Quantitative densitometric analysis was performed to normalize Nrf2, Keap1 and HO-1 expression levels from D (n=3). (G) Quantitative densitometric analysis was performed to normalize Nrf2 expression levels from E (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001 vs. CTL and LPS group separately. LPS, lipopolysaccharide; RT-qPCR, reverse transcription-quantitative PCR; ROS, reactive oxygen species; HO-1, heme oxygenase-1; WB, western blotting.
Antibody Against 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
https://www.bioz.com/result/antibody against nrf2/product/Proteintech
Average 96 stars, based on 1 article reviews
antibody against nrf2 - by Bioz Stars, 2026-02
96/100 stars
  Buy from Supplier

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CT alleviates UVA-induced ER stress and apoptosis via Nrf2 in HaCaT cells. (A) HaCaT cells were subjected to UVA radiation and treated with 50 or 100 μg/mL CT and/or siNrf2. Western blot assays were performed to detect the levels of ATF6, phosphorylated elF2a (p-elF2a), CHOP, GADD34, Cleaved caspase9, Cleaved caspase3, JNK, phosphorylated JNK (p-JNK), Bax, BCL2, cytoplasmic and nuclear NRF2 and HO-1. (B) Flow cytometry analysis was performed to determine cell apoptosis. Quantification of the percentage of apoptotic cells in different treatments. (C) Heatmap generated the data from RNAseq. Genes are all related to NRF2 downstream anti-oxidant or detoxification target genes. The figure was generated by SRplot . N = 4. * p ≤ 0.05; ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001.

Journal: Frontiers in Pharmacology

Article Title: Coreopsis tinctoria Nutt. attenuates ultraviolet A photodamage by suppressing endoplasmic reticulum stress-induced apoptosis via Nrf2 crosstalk

doi: 10.3389/fphar.2025.1686234

Figure Lengend Snippet: CT alleviates UVA-induced ER stress and apoptosis via Nrf2 in HaCaT cells. (A) HaCaT cells were subjected to UVA radiation and treated with 50 or 100 μg/mL CT and/or siNrf2. Western blot assays were performed to detect the levels of ATF6, phosphorylated elF2a (p-elF2a), CHOP, GADD34, Cleaved caspase9, Cleaved caspase3, JNK, phosphorylated JNK (p-JNK), Bax, BCL2, cytoplasmic and nuclear NRF2 and HO-1. (B) Flow cytometry analysis was performed to determine cell apoptosis. Quantification of the percentage of apoptotic cells in different treatments. (C) Heatmap generated the data from RNAseq. Genes are all related to NRF2 downstream anti-oxidant or detoxification target genes. The figure was generated by SRplot . N = 4. * p ≤ 0.05; ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001.

Article Snippet: After incubation with an endogenous peroxidase blocker (ZSGB-BIO, PV-6000), the slides were blocked with 3% BSA for 1 h. Primary antibodies against NRF2 (Proteintech, 16396-1-AP), Caspase12 (Proteintech, 55238-1-AP), and CHOP (Proteintech, 15204-1-AP) were incubated overnight at 4 °C at a dilution of 1:200 each.

Techniques: Western Blot, Flow Cytometry, Generated

Therapeutic effects of CT on macroscopic and histological changes induced by ER stress in UVA-photodamaged mouse skin. (A) Schematic representation of the experimental design for mice study. (B) Representative pictures of untreated or treated with UVA with CT or not. (C) Representative pictures of H&E and Masson staining of the skin of mice from different treatment groups on day 14. (D–F) Representative images of CHOP, NRF2, and caspase-12 for IHC analysis performed on skin sections of mice from different treatment groups on day 14.

Journal: Frontiers in Pharmacology

Article Title: Coreopsis tinctoria Nutt. attenuates ultraviolet A photodamage by suppressing endoplasmic reticulum stress-induced apoptosis via Nrf2 crosstalk

doi: 10.3389/fphar.2025.1686234

Figure Lengend Snippet: Therapeutic effects of CT on macroscopic and histological changes induced by ER stress in UVA-photodamaged mouse skin. (A) Schematic representation of the experimental design for mice study. (B) Representative pictures of untreated or treated with UVA with CT or not. (C) Representative pictures of H&E and Masson staining of the skin of mice from different treatment groups on day 14. (D–F) Representative images of CHOP, NRF2, and caspase-12 for IHC analysis performed on skin sections of mice from different treatment groups on day 14.

Article Snippet: After incubation with an endogenous peroxidase blocker (ZSGB-BIO, PV-6000), the slides were blocked with 3% BSA for 1 h. Primary antibodies against NRF2 (Proteintech, 16396-1-AP), Caspase12 (Proteintech, 55238-1-AP), and CHOP (Proteintech, 15204-1-AP) were incubated overnight at 4 °C at a dilution of 1:200 each.

Techniques: Staining

Cynarin suppresses macrophage-mediated inflammation through activation of the Nrf2-Keap1 signalling pathway. (A) RAW264.7 cells were exposed to cynarin (10, 50 or 100 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of IL1β , IL6 , Nos2 and Tnf were detected by RT-qPCR (n=3). (B) RAW264.7 cells and bone marrow-derived macrophages were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Intracellular ROS levels were measured with a ROS assay kit (n=3). (C) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 6 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of Nrf2 , Keap1 , Hmox1 and Cat were detected by RT-qPCR (n=3). (D) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Expression levels of Nrf2, Keap1 and HO-1 were detected by WB. (E) RAW264.7 cells were exposed to 100 μ M cynarin for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Nuclear extracts and cytoplasmic extracts were used to test expression of Nrf2 by WB. (F) Quantitative densitometric analysis was performed to normalize Nrf2, Keap1 and HO-1 expression levels from D (n=3). (G) Quantitative densitometric analysis was performed to normalize Nrf2 expression levels from E (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001 vs. CTL and LPS group separately. LPS, lipopolysaccharide; RT-qPCR, reverse transcription-quantitative PCR; ROS, reactive oxygen species; HO-1, heme oxygenase-1; WB, western blotting.

Journal: International Journal of Molecular Medicine

Article Title: Cynarin as a potent anti-osteolytic agent: Targeting MAPK and Nrf2-Keap1 pathways for osteoclast inhibition and bone protection

doi: 10.3892/ijmm.2025.5647

Figure Lengend Snippet: Cynarin suppresses macrophage-mediated inflammation through activation of the Nrf2-Keap1 signalling pathway. (A) RAW264.7 cells were exposed to cynarin (10, 50 or 100 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of IL1β , IL6 , Nos2 and Tnf were detected by RT-qPCR (n=3). (B) RAW264.7 cells and bone marrow-derived macrophages were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 12 h. Intracellular ROS levels were measured with a ROS assay kit (n=3). (C) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 6 h and then treated with LPS (1 μ g/ml) for 12 h. Expression levels of Nrf2 , Keap1 , Hmox1 and Cat were detected by RT-qPCR (n=3). (D) RAW264.7 cells were exposed to cynarin (10, 50, 100 or 200 μ M) for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Expression levels of Nrf2, Keap1 and HO-1 were detected by WB. (E) RAW264.7 cells were exposed to 100 μ M cynarin for 24 h and then treated with LPS (1 μ g/ml) for 24 h. Nuclear extracts and cytoplasmic extracts were used to test expression of Nrf2 by WB. (F) Quantitative densitometric analysis was performed to normalize Nrf2, Keap1 and HO-1 expression levels from D (n=3). (G) Quantitative densitometric analysis was performed to normalize Nrf2 expression levels from E (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001 vs. CTL and LPS group separately. LPS, lipopolysaccharide; RT-qPCR, reverse transcription-quantitative PCR; ROS, reactive oxygen species; HO-1, heme oxygenase-1; WB, western blotting.

Article Snippet: Antibodies against Nrf2 (cat. no. 16396-1-AP), Keap1 (cat. no. 10503-2-AP), osteocalcin (OCN; cat. no. 16157-1-AP), tumor necrosis factor-alpha (TNFα; cat. no. 17590-1-AP) and inducible nitric oxide synthase (iNOS; cat. no. 22226-1-AP) were sourced from Proteintech Group, Inc.

Techniques: Activation Assay, Expressing, Quantitative RT-PCR, Derivative Assay, ROS Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot

Cynarin suppresses osteoclastogenesis and inflammation via the MAPK and Nrf2-Keap1 pathways in inflammatory bone resorption. (A) Representative images of calvarial histology stained with Nrf2 and Keap1 (magnification, ×40, first row; ×200, second row; ×40, third row). (B) Representative images of calvarial histology stained with p-ERK1/2, p-JNK1/2 and p-P38 (magnification, ×100). (C) Quantitative analysis of the expression of Nrf2 and Keap1 in the immunofluorescence staining. (D) Quantitative analysis of the expression of p-ERK1/2, p-JNK1/2 and p-P38 in the immunohistochemical staining. All experiments were performed with three independent biological replicates (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001. p-, phosphorylated; Cy-M, medium-dose cynarin; LPS, lipopolysaccharide; Alen, alendronate.

Journal: International Journal of Molecular Medicine

Article Title: Cynarin as a potent anti-osteolytic agent: Targeting MAPK and Nrf2-Keap1 pathways for osteoclast inhibition and bone protection

doi: 10.3892/ijmm.2025.5647

Figure Lengend Snippet: Cynarin suppresses osteoclastogenesis and inflammation via the MAPK and Nrf2-Keap1 pathways in inflammatory bone resorption. (A) Representative images of calvarial histology stained with Nrf2 and Keap1 (magnification, ×40, first row; ×200, second row; ×40, third row). (B) Representative images of calvarial histology stained with p-ERK1/2, p-JNK1/2 and p-P38 (magnification, ×100). (C) Quantitative analysis of the expression of Nrf2 and Keap1 in the immunofluorescence staining. (D) Quantitative analysis of the expression of p-ERK1/2, p-JNK1/2 and p-P38 in the immunohistochemical staining. All experiments were performed with three independent biological replicates (n=3). The data are presented as the mean ± SD. * P<0.05, ** P<0.01 and **** P<0.0001. p-, phosphorylated; Cy-M, medium-dose cynarin; LPS, lipopolysaccharide; Alen, alendronate.

Article Snippet: Antibodies against Nrf2 (cat. no. 16396-1-AP), Keap1 (cat. no. 10503-2-AP), osteocalcin (OCN; cat. no. 16157-1-AP), tumor necrosis factor-alpha (TNFα; cat. no. 17590-1-AP) and inducible nitric oxide synthase (iNOS; cat. no. 22226-1-AP) were sourced from Proteintech Group, Inc.

Techniques: Staining, Expressing, Immunofluorescence, Immunohistochemical staining