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ampk inhibitor dorsomorphin  (MedChemExpress)


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    MedChemExpress ampk inhibitor dorsomorphin
    Biogenic SeNPs regulated <t>AMPK/NLRP3/Nrf2</t> signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Ampk Inhibitor Dorsomorphin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 816 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 816 article reviews
    ampk inhibitor dorsomorphin - by Bioz Stars, 2026-02
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    1) Product Images from "Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip"

    Article Title: Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip

    Journal: Journal of Advanced Research

    doi: 10.1016/j.jare.2025.04.023

    Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Staining, Activity Assay, In Vitro

    Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to attenuate oxidative stress-induced intestinal barrier dysfunction and mast cell overactivation in mice. A. Immunofluorescence analysis of p-AMPK (red), NLRP3 (yellow) and Nrf2 (green) in jejunum of mice with different treatments (Scale bar: 100 μm). B. Western blot analysis of pAMPK and Nrf2 expression levels in mice jejunum. C. Western blot analysis of NLRP3 and its downstream pyroptosis-related protein expression levels in mice jejunum. Data are expressed as mean ± S.E.M. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001.
    Figure Legend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to attenuate oxidative stress-induced intestinal barrier dysfunction and mast cell overactivation in mice. A. Immunofluorescence analysis of p-AMPK (red), NLRP3 (yellow) and Nrf2 (green) in jejunum of mice with different treatments (Scale bar: 100 μm). B. Western blot analysis of pAMPK and Nrf2 expression levels in mice jejunum. C. Western blot analysis of NLRP3 and its downstream pyroptosis-related protein expression levels in mice jejunum. Data are expressed as mean ± S.E.M. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Techniques Used: Immunofluorescence, Western Blot, Expressing



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    Biogenic SeNPs regulated <t>AMPK/NLRP3/Nrf2</t> signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.
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    Image Search Results


    Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Journal of Advanced Research

    Article Title: Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip

    doi: 10.1016/j.jare.2025.04.023

    Figure Lengend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to alleviate intestinal epithelial barrier oxidative damage in gut-on-a-chip. A. Schematic diagram of experimental design. B. pAMPK/NLRP3/Nrf2 immunofluorescent staining (Scale bar: 40 μm). C. Villi-like height. D. LDH activity in the upper channel layer. E. IL-1β levels in the upper channel layer. F. IL-18 levels in the upper channel layer. G. Schematic diagram of the mechanism by which SeNPs exert antioxidant effects against oxidative damage to intestinal epithelial cells in vitro . Data are expressed as mean ± S.E.M. n = 4. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: To investigate the role of the AMPK signaling pathway in the protection of the intestinal epithelial barrier from oxidative stress damage by SeNPs, AMPK activator AICAR (MedChemExpres; Cat# HY-13417) and AMPK inhibitor Dorsomorphin (MedChemExpres; Cat# HY-13418A) were introduced into the gut-on-a-chip, respectively.

    Techniques: Staining, Activity Assay, In Vitro

    Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to attenuate oxidative stress-induced intestinal barrier dysfunction and mast cell overactivation in mice. A. Immunofluorescence analysis of p-AMPK (red), NLRP3 (yellow) and Nrf2 (green) in jejunum of mice with different treatments (Scale bar: 100 μm). B. Western blot analysis of pAMPK and Nrf2 expression levels in mice jejunum. C. Western blot analysis of NLRP3 and its downstream pyroptosis-related protein expression levels in mice jejunum. Data are expressed as mean ± S.E.M. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Journal of Advanced Research

    Article Title: Prophylactic supplementation with biogenic selenium nanoparticles mitigated intestinal barrier oxidative damage through suppressing epithelial-immune crosstalk with gut-on-a-chip

    doi: 10.1016/j.jare.2025.04.023

    Figure Lengend Snippet: Biogenic SeNPs regulated AMPK/NLRP3/Nrf2 signaling pathway to attenuate oxidative stress-induced intestinal barrier dysfunction and mast cell overactivation in mice. A. Immunofluorescence analysis of p-AMPK (red), NLRP3 (yellow) and Nrf2 (green) in jejunum of mice with different treatments (Scale bar: 100 μm). B. Western blot analysis of pAMPK and Nrf2 expression levels in mice jejunum. C. Western blot analysis of NLRP3 and its downstream pyroptosis-related protein expression levels in mice jejunum. Data are expressed as mean ± S.E.M. n = 3. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: To investigate the role of the AMPK signaling pathway in the protection of the intestinal epithelial barrier from oxidative stress damage by SeNPs, AMPK activator AICAR (MedChemExpres; Cat# HY-13417) and AMPK inhibitor Dorsomorphin (MedChemExpres; Cat# HY-13418A) were introduced into the gut-on-a-chip, respectively.

    Techniques: Immunofluorescence, Western Blot, Expressing

    Gin A activates AMPK and suppresses mTOR/S6K1 signaling in A10 cells (A) Concentration-dependent effects of Gin A on AMPK phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-AMPK/AMPK ratios were determined by Western blot. (B) Time course of AMPK activation by Gin A. Cells were exposed to Gin A (10 μM) for 0.5, 1, 3, 6 or 24 h, and p-AMPK/AMPK levels were determined by Western blot. (C) Effects of Gin A on mTOR phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-mTOR/mTOR ratios were determined by Western blot. (D) Effects of Gin A on S6K1 phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-S6K1/S6K1 ratios determined by Western blot (n = 6; * P < 0.05 vs. control).

    Journal: Frontiers in Pharmacology

    Article Title: Gingerenone A attenuates diabetic vascular remodeling through AMPK/mTOR/S6K1 signaling

    doi: 10.3389/fphar.2026.1706103

    Figure Lengend Snippet: Gin A activates AMPK and suppresses mTOR/S6K1 signaling in A10 cells (A) Concentration-dependent effects of Gin A on AMPK phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-AMPK/AMPK ratios were determined by Western blot. (B) Time course of AMPK activation by Gin A. Cells were exposed to Gin A (10 μM) for 0.5, 1, 3, 6 or 24 h, and p-AMPK/AMPK levels were determined by Western blot. (C) Effects of Gin A on mTOR phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-mTOR/mTOR ratios were determined by Western blot. (D) Effects of Gin A on S6K1 phosphorylation. A10 cells were treated with Gin A at 0.1, 1, 10 or 100 μM for 24 h, and p-S6K1/S6K1 ratios determined by Western blot (n = 6; * P < 0.05 vs. control).

    Article Snippet: A10 cells were co-treated with Gin A and the pharmacological AMPK inhibitor Compound C (HY-13418A, MCE, United States) under HG (30 mM) stimulation.

    Techniques: Concentration Assay, Phospho-proteomics, Western Blot, Activation Assay, Control

    Role of AMPK activation in the Gin A-mediated inhibition of the proliferation and migration of HG-treated A10 cells (A) Effect of the AMPK inhibitor Compound C on Gin A-induced AMPK activation in HG-treated A10 cells. Cells were pre-incubated with Compound C for 1 h and then exposed to HG (30 mM) with or without Gin A (10 μM) for 24 h. Representative blots and p-AMPK/AMPK ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. Gin A alone). (B–D) Effects of Compound C on the Gin A-induced inhibition of A10 cell proliferation and migration. Cell proliferation was determined by the MTT assay (B) . Cell migration was determined by Transwell (C) and wound healing (D) assays (n = 8; * P < 0.05 vs. control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A). (E,F) Effects of Compound C on Gin A-mediated inhibition of mTOR/S6K1 signaling in HG-treated A10 cells. Representative blots and quantification of p-mTOR/mTOR (E) and p-S6K1/S6K1 (F) ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A).

    Journal: Frontiers in Pharmacology

    Article Title: Gingerenone A attenuates diabetic vascular remodeling through AMPK/mTOR/S6K1 signaling

    doi: 10.3389/fphar.2026.1706103

    Figure Lengend Snippet: Role of AMPK activation in the Gin A-mediated inhibition of the proliferation and migration of HG-treated A10 cells (A) Effect of the AMPK inhibitor Compound C on Gin A-induced AMPK activation in HG-treated A10 cells. Cells were pre-incubated with Compound C for 1 h and then exposed to HG (30 mM) with or without Gin A (10 μM) for 24 h. Representative blots and p-AMPK/AMPK ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. Gin A alone). (B–D) Effects of Compound C on the Gin A-induced inhibition of A10 cell proliferation and migration. Cell proliferation was determined by the MTT assay (B) . Cell migration was determined by Transwell (C) and wound healing (D) assays (n = 8; * P < 0.05 vs. control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A). (E,F) Effects of Compound C on Gin A-mediated inhibition of mTOR/S6K1 signaling in HG-treated A10 cells. Representative blots and quantification of p-mTOR/mTOR (E) and p-S6K1/S6K1 (F) ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A).

    Article Snippet: A10 cells were co-treated with Gin A and the pharmacological AMPK inhibitor Compound C (HY-13418A, MCE, United States) under HG (30 mM) stimulation.

    Techniques: Activation Assay, Inhibition, Migration, Incubation, Control, MTT Assay

    Experimental validation in primary HASMCs with siRNA knockdown and osmotic stress controls (A) Confirmation of AMPK knockdown in primary HASMCs. Representative western blots and AMPK/GAPDH ratios in scrambled siRNA- and AMPK siRNA-transfected cells are shown (n = 6; * P < 0.05 vs. control). (B) Effects of Gin A (10 μM) and AMPK knockdown on AMPK phosphorylation in HASMCs exposed to HG (25 mM) for 24 h. Representative blots and p-AMPK/GAPDH ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. si-AMPK alone; & P < 0.05 vs. si-AMPK + Gin A). (C) Effects of Gin A and AMPK knockdown on HG-induced HASMC proliferation. Cells were exposed to normal glucose or HG (25 mM) with or without Gin A (10 μM) and with scrambled or AMPK-targeting siRNA, and proliferation was measured by MTT assay (n = 6; * P < 0.05 vs. normal-glucose control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A with scrambled siRNA). (D) Osmotic control experiments in HASMCs. Cells were cultured for 24 h in normal glucose (5.5 mM), HG (25 mM), L-glucose (25 mM) or D-mannitol (25 mM), and proliferation was assessed by MTT assay (n = 6; * P < 0.05 vs. normal-glucose control).

    Journal: Frontiers in Pharmacology

    Article Title: Gingerenone A attenuates diabetic vascular remodeling through AMPK/mTOR/S6K1 signaling

    doi: 10.3389/fphar.2026.1706103

    Figure Lengend Snippet: Experimental validation in primary HASMCs with siRNA knockdown and osmotic stress controls (A) Confirmation of AMPK knockdown in primary HASMCs. Representative western blots and AMPK/GAPDH ratios in scrambled siRNA- and AMPK siRNA-transfected cells are shown (n = 6; * P < 0.05 vs. control). (B) Effects of Gin A (10 μM) and AMPK knockdown on AMPK phosphorylation in HASMCs exposed to HG (25 mM) for 24 h. Representative blots and p-AMPK/GAPDH ratios are shown (n = 6; * P < 0.05 vs. control; # P < 0.05 vs. si-AMPK alone; & P < 0.05 vs. si-AMPK + Gin A). (C) Effects of Gin A and AMPK knockdown on HG-induced HASMC proliferation. Cells were exposed to normal glucose or HG (25 mM) with or without Gin A (10 μM) and with scrambled or AMPK-targeting siRNA, and proliferation was measured by MTT assay (n = 6; * P < 0.05 vs. normal-glucose control; # P < 0.05 vs. HG alone; & P < 0.05 vs. HG + Gin A with scrambled siRNA). (D) Osmotic control experiments in HASMCs. Cells were cultured for 24 h in normal glucose (5.5 mM), HG (25 mM), L-glucose (25 mM) or D-mannitol (25 mM), and proliferation was assessed by MTT assay (n = 6; * P < 0.05 vs. normal-glucose control).

    Article Snippet: A10 cells were co-treated with Gin A and the pharmacological AMPK inhibitor Compound C (HY-13418A, MCE, United States) under HG (30 mM) stimulation.

    Techniques: Biomarker Discovery, Knockdown, Western Blot, Transfection, Control, Phospho-proteomics, MTT Assay, Cell Culture

    Gin A attenuates neointimal hyperplasia and restores AMPK activation in diabetic rats after carotid balloon injury (A) Representative H&E-stained cross-sections of carotid arteries from Sham, Vehicle and Gin A-treated diabetic rats 2 weeks after balloon injury (or sham operation). (B) Quantitative analysis of the intima-to-media (I/M) ratio in carotid arteries from the indicated groups. (C) Effects of Gin A on PCNA expression levels in carotid arteries of diabetic rats. Representative western blots and PCNA/H3 ratios are shown. (D,E) Effects of Gin A on oxidative stress markers in carotid arteries of diabetic rats. MDA (D) and T-AOC (E) measured in vascular tissue lysates. (F) Effects of Gin A on AMPK activation in carotid arteries of diabetic rats. Representative western blots and quantification of p-AMPK/AMPK ratios in carotid arteries are shown, indicating the restoration of AMPK activation by Gin A (n = 6; * P < 0.05 vs. Sham; # P < 0.05 vs. Vehicle).

    Journal: Frontiers in Pharmacology

    Article Title: Gingerenone A attenuates diabetic vascular remodeling through AMPK/mTOR/S6K1 signaling

    doi: 10.3389/fphar.2026.1706103

    Figure Lengend Snippet: Gin A attenuates neointimal hyperplasia and restores AMPK activation in diabetic rats after carotid balloon injury (A) Representative H&E-stained cross-sections of carotid arteries from Sham, Vehicle and Gin A-treated diabetic rats 2 weeks after balloon injury (or sham operation). (B) Quantitative analysis of the intima-to-media (I/M) ratio in carotid arteries from the indicated groups. (C) Effects of Gin A on PCNA expression levels in carotid arteries of diabetic rats. Representative western blots and PCNA/H3 ratios are shown. (D,E) Effects of Gin A on oxidative stress markers in carotid arteries of diabetic rats. MDA (D) and T-AOC (E) measured in vascular tissue lysates. (F) Effects of Gin A on AMPK activation in carotid arteries of diabetic rats. Representative western blots and quantification of p-AMPK/AMPK ratios in carotid arteries are shown, indicating the restoration of AMPK activation by Gin A (n = 6; * P < 0.05 vs. Sham; # P < 0.05 vs. Vehicle).

    Article Snippet: A10 cells were co-treated with Gin A and the pharmacological AMPK inhibitor Compound C (HY-13418A, MCE, United States) under HG (30 mM) stimulation.

    Techniques: Activation Assay, Staining, Expressing, Western Blot