Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of AdipoRon intervention on the expression of key adiponectin signaling molecules that regulate lipid metabolism in mixed fatty acid (OA + PA)-treated LMH cells. (A) Relative mRNA expression of AdipoR1, AdipoR2, PPARα, and AMPK. (B) Protein expression of AdipoR1, AdipoR2, PPARα, and AMPK. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+LA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 20 μM AdipoRon-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+HA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 60 μM AdipoRon-treated group; OA, oleic acid; PA, palmitic acid; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; PPARα, peroxisome proliferator-activated receptor-α; AMPK, adenosine 5′-monophosphate-activated protein kinase. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the AdipoRon-mediated mitigation of lipotoxicity-induced injury in LMH cells. (A) Oil Red O staining results for LMH cells. (B) TG and TC contents in LMH cells. (C) GPT and GOT activity levels in LMH cells. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; TG, triglyceride; TC, total cholesterol; GPT, glutamic pyruvic transaminase; GOT, glutamic oxaloacetic transaminase. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Staining, Activity Assay, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the mRNA expression of lipid metabolism-related genes in LMH cells. (A) Lipid synthesis-related genes. (B) Fatty acid β-oxidation-related genes. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; ACC, acetyl-CoA carboxylase; SCD-1, stearyl coenzyme A dehydrogenase-1; ACOX-1, acyl-CoA oxidase 1; CPT-1, carnitine palmitoyltransferase 1. All the data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on the expression of key signaling molecules of adiponectin that regulate lipid metabolism in LMH cells. (A) Relative mRNA expression of AdipoR1, AdipoR2, and AMPK. (B) Protein expression of AdipoR1, AdipoR2, AMPK, and p-AMPK. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; OA, oleic acid; PA, palmitic acid; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; AMPK, adenosine 5′-monophosphate-activated protein kinase. All data are expressed as the mean±SEM. * indicates P <0.05; ** indicates P <0.01; *** indicates P <0.001; ⁎⁎⁎⁎ indicates P <0.0001.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Effects of inhibiting and activating AMPK signaling on lipid components in LMH cells. (A) Z score plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The Z score plot normalizes differential lipid molecules across different samples by calculating Z score values. The calculation formula is z=(x-μ)/σ, where x represents a specific score, μ denotes the mean, and σ indicates the standard deviation. The horizontal axis displays Z score values, the vertical axis shows differential lipids, and the differently colored points indicate samples from different groups. (B) Heatmap plot for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents different experimental groups, whereas the vertical axis denotes the differentially expressed lipid molecules within each group. The expression level of each lipid is indicated by a color gradient, with darker shades reflecting greater statistical significance. Color blocks at different positions represent the relative expression levels of corresponding lipid molecules at those positions: red indicates high expression of the substance in that group, while blue indicates low expression. (C) KEGG pathway annotation classification diagram for Group C vs. Group H vs. Group H+MA vs. Group H+MA+A vs. Group H+MA+C. The horizontal axis represents the enrichment ratio for each pathway, while the vertical axis displays the names of the metabolic pathways. Colors indicate the magnitude of p values, with redder hues corresponding to smaller p values, signifying more significant enrichment. Abbreviations: C, control group; H, mixed fatty acid (0.30 mM OA + 0.15 mM PA)-treated group; H+MA, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon-treated group; H+MA+A, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 0.5 mM AICAR-treated group; H+MA+C, mixed fatty acid (0.30 mM OA + 0.15 mM PA) + 40 μM AdipoRon + 10 μM Compound C-treated group; OA, oleic acid; PA, palmitic acid; TAG, triacylglycerol; PG, phosphatidylglycerol; PetOH, phosphatidylethanol; PE, phosphatidylethanolamine; PC, phosphatidylcholine; HexCer-NS, hexosylceramide nonhydroxyfatty acid-sphingosine; HexCer-AP, hexosylceramide alpha-hydroxy fatty acid-phytosphingosine; GlcADG, glucuronosyldiacylglycerol; Cer-AP, ceramide alpha-hydroxy fatty acid-phytosphingosine; ACar, acylcarnitine.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Standard Deviation, Expressing, Control

Journal: Poultry Science

Article Title: The adiponectin receptor agonist AdipoRon alleviates lipotoxic injury in LMH cells

doi: 10.1016/j.psj.2026.106573

Figure Lengend Snippet: Schematic diagram illustrating the molecular mechanism through which AdipoRon mitigates mixed fatty acid (OA + PA)-induced lipotoxicity in LMH cells. AdipoRon activates AMPK and PPARα signaling by binding to AdipoR1 and AdipoR2 on the LMH cell membrane, thereby downregulating the expression of the lipid synthesis-related genes ACC, FAS, SCD-1, and SREBP-1 and upregulating the expression of the fatty acid oxidation-related genes ACOX-1 and CPT-1. It subsequently regulates SP, GP, ACar, and GL metabolism; reduces cellular levels of Cer, SM, TAG, and ACar; and maintains the metabolic homeostasis of PE and PC, as well as cell membrane structural integrity and functional stability. Finally, it mitigates lipotoxic injury induced by mixed fatty acids (OA + PA) in LMH cells. Abbreviations: AMPK, adenosine 5′-monophosphate-activated protein kinase; PPARα, peroxisome proliferator-activated receptor-α; AdipoR1, adiponectin receptor 1; AdipoR2, adiponectin receptor 2; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthetase; SCD-1, stearyl coenzyme A dehydrogenase-1; SREBP-1, sterol regulatory element-binding protein 1; ACOX-1, acyl-CoA oxidase 1; CPT-1, carnitine palmitoyltransferase 1; SP, sphingolipid; GP, glycerophospholipid; ACar, acylcarnitine; GL, glycerolipid; Cer, ceramide; SM, sphingomyelin; TAG, triacylglycerol; PE, phosphatidylethanolamine; PC, phosphatidylcholine; glycosphingolipids; OA, oleic acid; PA, palmitic acid; LMH, leghorn male hepatoma.

Article Snippet: To determine whether AdipoRon alleviates mixed fatty acid-induced lipotoxic injury in LMH cells via AMPK signaling, the cells were grouped and treated as follows: cells in the control group (Group C) were cultured in normal serum-free medium; cells in the model group (Group H) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA); cells in the fatty acid + medium AdipoRon group (Group H+MA) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA) and 40 μM AdipoRon; cells in the AMPK antagonist Compound C group (Group H+MA+C) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 10 μM Compound C (Cat# HY-13418A, MedChemExpress); and cells in the AMPK agonist Acadesine (AICAR) group (Group H+MA+A) were cultured in serum-free medium supplemented with mixed fatty acids (0.30 mM OA + 0.15 mM PA), 40 μM AdipoRon, and 0.5 mM AICAR (Cat# HY-13417, MedChemExpress).

Techniques: Binding Assay, Membrane, Expressing, Functional Assay

Journal: Scientific Reports

Article Title: Organophosphate pesticide DEDT promotes diabetic retinopathy progression via AMPK/Nrf2/HO-1 pathway

doi: 10.1038/s41598-026-37183-w

Figure Lengend Snippet: AICAR-mediated AMPK activation rescues DEDT-induced retinal damage. ( A ) The effect of the AMPK activator AICAR on retinal cell viability under high glucose conditions with DEDT exposure. ( B ) Quantitative PCR was performed to analyze the mRNA expression of key components in the AMPK/Nrf2/HO-1 signaling pathway. ( C-D ) Protein levels of AMPK, Nrf2, and HO-1 were quantified by WB and quantitative analysis. ( E ) The expression of the anti-apoptotic protein BCL-2 was evaluated using ELISA. ( F-G ) Levels of tight junction proteins. ( H ) Inflammatory cytokines, including IL-6 and IL-8, were quantified by ELISA. All DEDT treatments were conducted under high-glucose exposure. Data are presented as mean ± SD ( n = 6). Statistical significance was determined by one-way ANOVA followed by Tukey’s post-hoc test, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05, ns = not significant. AICAR: AMPK activator.

Article Snippet: Streptozotocin (STZ), Catalog: S0130, Sigma-Aldrich; Diethyl Dithiophosphate (DEDT), Catalog: 24617-47-0, ChemService; AICAR, Catalog: 99447-33-3, Tocris Bioscience; Cell Counting Kit-8 (CCK-8), Catalog: C0037, Beyotime Biotechnology; TRIzol Reagent, Catalog: 15,596,026, Thermo Fisher Scientific; SYBR Green Master Mix, Catalog: 4,309,155, Applied Biosystems; Cell Counting Kit-8 (CCK-8), Catalog: C0037, Beyotime Biotechnology; ZO-1 ELISA Kit, Catalog: PT518, Beyotime Biotechnology; Occludin ELISA Kit, Catalog: PT519, Beyotime Biotechnology; Claudin-5 ELISA Kit, Catalog: PT521, Beyotime Biotechnology; IL-6 ELISA Kit, Catalog: PI330, Beyotime Biotechnology; TNF-α ELISA Kit, Catalog: PI305, Beyotime Biotechnology;; IL-8 ELISA Kit, Catalog: PI331, Beyotime Biotechnology;; IL-1β ELISA Kit, Catalog: PI303, Beyotime Biotechnology; Bax ELISA Kit, Catalog: PA102, Beyotime Biotechnology; BCL-2 ELISA Kit, Catalog: PA101, Beyotime Biotechnology; Phospho-AMPK (Thr172) ELISA Kit, Catalog: PT428, Beyotime Biotechnology; Nrf2 ELISA Kit, Catalog: PT588, Beyotime Biotechnology; HO-1 ELISA Kit, Catalog: PT592, Beyotime Biotechnology; Glutathione (GSH) Assay Kit, Catalog: S0053, Beyotime Biotechnology; Malondialdehyde (MDA) test kit, Catalog: S0131S, Beyotime Biotechnology; Superoxide dismutase (SOD) test kit, Catalog: S0101, Beyotime Biotechnology; Catalase (CAT) test kit, Catalog: S0051, Beyotime Biotechnology.

Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Expressing, Enzyme-linked Immunosorbent Assay

Journal: Cell Death & Disease

Article Title: AURKA-mediated destabilization of SAPS3 drives ferroptosis evasion via 7-dehydrocholesterol biosynthesis in colorectal cancer

doi: 10.1038/s41419-026-08549-9

Figure Lengend Snippet: A Venn diagram analysis of transcription factors predicated to regulate DHCR7 gene transcription based on ChIP-Atlas, GTRD, and hTFtarget databases. B Western blot analysis of SREBP2, c-Myc, ZEB1, and MAX in CRC (shNC and sh AURKA ) cells. C Western blot analysis of SREBP2 and DHCR7 protein levels in SW480 cells after siRNA-mediated SREBP2 knockdown. D qPCR quantification of cholesterol biosynthesis enzyme mRNA levels in SREBP2-silenced SW480 cells. E IC 50 analysis of RSL3 in SREBP2-silenced SW480 (shNC and sh AURKA ) cells treated with RSL3 (48 h). F , G Representative FACS images and quantified values of lipid ROS levels ( F ) and GSH/GSSG ratios ( G ) in SREBP2-silenced SW480 (shNC and sh AURKA ) cells treated with RSL3 (5 μM, 24 h). H , I Western blot analysis of SREBP2 at indicated timepoints after CHX (100 µg/ml) treatment ( H ), and quantified degradation kinetics ( I ) in SW480 cells. J Immunofluorescence (IF) analyses of subcellular distribution of SREBP2 in SW480 (shNC and sh AURKA ) cells. K , L Western blot analysis of pSREBP2, nSREBP2, total AMPK, and pAMPK levels in SW480 (shNC and sh AURKA ) cells ( K ) and post AICAR treatment (1 mM, 24 h, L ). M IC 50 analysis of RSL3 in SW480 (shNC and sh AURKA ) cells after pretreatment with AICAR (1 mM, 24 h). N Representative FACS images and quantified values of lipid ROS levels in SW480 (shNC and sh AURKA ) cells treated with AICAR (1 mM, 24 h). Data are presented as mean ± SD from at least three independent experiments. Statistical analyses were performed using unpaired Student’s t test [( D ), ( F ), ( G ), and ( N )]. ** p < 0.01, *** p < 0.001.

Article Snippet: RSL3 (S8155), Erastin (S7242), FIN56 (S8254), 5-Fluorouracil (S1209), Oxaliplatin (S1224), Alisertib (S1133), AICAR (S1802), and Bafilomycin A1 (S1413) were obtained from Selleck (Houston, USA).

Techniques: Western Blot, Knockdown, Immunofluorescence