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

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

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

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

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: Research

Article Title: A Novel Autophagy Inhibitor p -Hydroxylcinnamaldehyde Suppresses Esophageal Squamous Cell Carcinoma by Targeting LDHA Phosphorylation-Mediated Metabolic Reprogramming

doi: 10.34133/research.1070

Figure Lengend Snippet: CMSP reduces AMPK/mTOR pathway activity in ESCC cells. (A) AMP, ATP, and ratio of AMP and ATP response to CMSP treatment in targeted metabolomics. (B) Representative Western blot of p-mTOR, mTOR, p-AMPK, AMPK, p-P70S6K, P70S6K, p-ULK1, and ULK1 following treatment of concentration-dependent CMSP for 36 h. (C) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K, and p-ULK1 following treatment of CMSP (40 μg/ml) for different time. (D) Representative Western blot of p-mTOR, p-AMPK, p-P70S6K and p-ULK1 following treatment of CMSP (40 μg/ml) and rapamycin (20 nM). Data are shown as the mean ± SD ( n = 3); Student’s t test; ** P < 0.01 versus the control group.

Article Snippet: Antibodies against actin (20536-1-AP), LC3B (14600-1-AP), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (10494-1-AP), p-mTOR (67778-1-Ig), mTOR (66888-1-Ig), AMPK (66536-1-Ig), P70S6K (14485-1-AP), and ULK1 (20986-1-AP) were purchased from Proteintech Group (Wuhan, China).

Techniques: Activity Assay, Western Blot, Concentration Assay, Control

Journal: Food Science & Nutrition

Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

doi: 10.1002/fsn3.71429

Figure Lengend Snippet: AYN activated AMPKα pathway in tissues. (A) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in epWAT; (B) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in epWAT; (C) AYN intervention increased p‐AMPKα, GLUT4, and CPT‐1α expression in skeletal muscles; (D) Relative band intensity for GLUT4/β‐Actin, CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in skeletal muscles. (E) AYN intervention increased p‐AMPKα and CPT‐1α expression in livers; (F) Relative band intensity for CPT‐1α/β‐Actin, p‐AMPKα/AMPKα for protein in livers. ( n = 3, +++ p < 0.001, compared with Normal control group; * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Vehicle control group).

Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

Techniques: Expressing, Muscles, Control

Journal: Food Science & Nutrition

Article Title: Anti‐Diabetic Effects of Ayanin, a Flavonoid Compound, in STZ / HFD ‐Induced Diabetic Mice by Upregulating GLUT4 and Suppressing Macrophage‐Driven Inflammation in Adipose Tissues

doi: 10.1002/fsn3.71429

Figure Lengend Snippet: AYN increased glucose uptake of 3T3‐L1 adipocytes by activating AMPKα/GLUT4 pathway. (A) AYN increased GLUT4 and p‐AMPKα expression in 3T3‐L1 adipocytes; (B) Relative band intensity for GLUT4/β‐Actin, p‐AMPKα/AMPKα for protein in 3T3‐L1 adipocytes; (C) AYN increased the glucose uptake of 3T3‐L1 adipocytes; (D) AMPKα inhibitor, Compound C, suppressed the GLUT4 expression of 3T3‐L1 adipocytes induced by AYN; (E) Compound C inhibited the glucose uptake of 3T3‐L1 adipocytes induced by AYN. ( n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, compared with Normal control group; +++ p < 0.001, compared with AYN group in E).

Article Snippet: Antibodies of β‐actin, GLUT4, Cpt‐1α, AMPKα, p‐AMPKα and corresponding secondary antibodies were purchased from Proteintech Group (Wuhan, China).

Techniques: Expressing, Control