ampk inhibitor compound c  (MedChemExpress)

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

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

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

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

Journal: Advanced Science

Article Title: Trigonelline Improves Metabolism and Cardiac Function of HFpEF Mice Via Gut Microbiome Alterations‐Mediated AMPK Activation

doi: 10.1002/advs.202513956

Figure Lengend Snippet: AMPK activation was required for the cardioprotective effects of trigonelline in HFpEF mice. A) Representative immunoblot images of total and phosphorylated AMPK in the heart and liver tissues from HFpEF mice receiving trigonelline. B,C) Quantification of cardiac p‐AMPK/AMPK ( n = 6 mice per group). D) Representative immunoblot images of total and phosphorylated AMPK in the heart and liver tissues from HFpEF mice receiving trigonelline with or without AMPK inhibitor. E,F) Quantification of hepatic p‐AMPK/AMPK ratio ( n = 6 mice per group). G,H) SBP and DBP of different experimental groups ( n = 5 mice per group). I) Representative echocardiography‐derived M‐mode tracings (top), pulsed‐wave Doppler (middle), and tissue Doppler (bottom) tracings of mice in the indicated group. J) Percent left ventricular ejection fraction (LVEF%). K) The ratio between mitral E wave and E’ wave (E/E’). L) Running distance during the exercise exhaustion test of mice. M) The ratio between wet and dry lung weight (LW). N) Ratio between heart weight and tibia length (HW/TL) (for LVEF%, E/E’ ratio, running distance, LW wet/LW dry ratio, and HW/TL ratio, n = 6 mice per group). O) Representative images of WGA in transversal sections of the left ventricle of mice of different experimental groups. Scale bar: 50 µm for WGA. P) WGA quantification of cardiomyocyte cross‐sectional area ( n = 5 mice per group). Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Tukey's multiple comparisons test. ns, no significant; * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001.

Article Snippet: To test the role of AMPK in the therapeutic effects of trigonelline in vivo, HFpEF mice were pre‐treated with AMPK inhibitor Compound C (CC) (MedChemExpress, HY‐13418, 5 mg kg −1 day −1 ) or vehicle for 1 week.

Techniques: Activation Assay, Western Blot, Derivative Assay

Journal: Advanced Science

Article Title: Trigonelline Improves Metabolism and Cardiac Function of HFpEF Mice Via Gut Microbiome Alterations‐Mediated AMPK Activation

doi: 10.1002/advs.202513956

Figure Lengend Snippet: AMPK inhibition abolished the beneficial effects of trigonelline on metabolic disorders in HFpEF mice. A) Food intake of mice per day of different experimental groups per day ( n = 5). B) Body weight was monitored weekly in each experimental group. C) Representative images of MRI of mice from different experimental groups. Red indicates higher fat content, green represents moderate fat content, and blue corresponds to low fat content. Scale bar: 1 cm. Fat mass D) and lean mass E) ratios of mice in the indicated groups ( n = 5). F) Glucose tolerance tests in the indicated groups ( n = 5). G) Insulin sensitivity tests in the indicated groups ( n = 5). H) Total cholesterol of serum in each group. I) Low‐density lipoprotein cholesterol (LDL‐C) of the serum in each group. J) Representative images of hematoxylin and eosin staining and oil red staining of liver from mice in each treated group, Scale bar = 100 µm. K) Serum ALT in each group. L) Serum AST in each group. M) Serum Cre in each group. N) Serum BUN in each group (for total cholesterol, LDL‐C, Serum ALT, AST, Cre, and BUN, n = 5 mice per group). Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Tukey's multiple comparisons test. ns, no significant; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Article Snippet: To test the role of AMPK in the therapeutic effects of trigonelline in vivo, HFpEF mice were pre‐treated with AMPK inhibitor Compound C (CC) (MedChemExpress, HY‐13418, 5 mg kg −1 day −1 ) or vehicle for 1 week.

Techniques: Inhibition, Staining

Journal: Advanced Science

Article Title: Trigonelline Improves Metabolism and Cardiac Function of HFpEF Mice Via Gut Microbiome Alterations‐Mediated AMPK Activation

doi: 10.1002/advs.202513956

Figure Lengend Snippet: Trigonelline activates AMPK in a gut microbiota‐dependent manner. A–C) Diversity of the gut microbiota in each group, as indicated by the observed species, Shannon, and Chao1 indices. D) PCA score plot analysis based on the relative abundance of OTUs. E) Scheme for the experimental strategy in HFpEF mice treated with trigonelline and antibiotics. F) Representative immunoblot images of total and phosphorylated AMPK in the heart and liver tissues of mice in each group. Quantification of cardiac pAMPK/AMPK ratio in the heart G) and liver H) tissues of mice in each group. ( n = 6 mice per group). I) Representative immunoblot images of total and phosphorylated AMPK in HL‐1 and HepG2 cell lines in each group. Quantification of cardiac pAMPK/AMPK ratio in the HL‐1 J) and HepG2 cell lines K) in each group. ( n = 4 mice per group). Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Tukey's multiple comparisons test. ns, no significant; * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Abx, antibiotic cocktail.

Article Snippet: To test the role of AMPK in the therapeutic effects of trigonelline in vivo, HFpEF mice were pre‐treated with AMPK inhibitor Compound C (CC) (MedChemExpress, HY‐13418, 5 mg kg −1 day −1 ) or vehicle for 1 week.

Techniques: Western Blot