Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2024-04-01
Abstract： Objective To investigate the effects and molecular mechanism of recombinant human adiponectin (APN) on arsenic induced lipid deposition in hepatic HepG-2 cells. Methods The experiments were divided into control group, sodium arsenite (SA) exposure group, rAPN intervention + SA exposure group, and protein kinase B (AKT) inhibitor (GSK690693) intervention + SA exposure group. After cultured HepG-2 cells in vitro were treated respectively, the characteristics of cellular lipid deposition were observed by oil red O staining of cells smears, and the methods of biochemical or enzyme-linked immunosorbent assay (ELISA) were applied to determine the levels of intracellular mitochondrial membrane potential (ΔΨm), mitochondrial carnitine palmitoyltransferase-1 (CPT-1) activity, free fatty acids (FFAs) and APN. Western-blotting (WB) was applied to detect the levels of phosphorylated AKT (p-AKT), mitochondrial Glutathione S-transferase K1 (GSTK1) and inflammatory factor Caspase-1. Results Compared with control group, SA exposed group showed intracellular lipid deposition and the decreased levels of mitochondria ΔΨm, CPT1 activity, GSTK1 or APN, while the levels of FFAs, p-AKT and Caspase-1 increased. Compared with SA exposed group, recombinant human APN (rAPN) intervention led to the alleviated lipid deposition in hepatocytes and the increased levels of ΔΨm, CPT1 activity, GSTK1 or APN, while the levels of FFAs, p-AKT and Caspase-1 decreased. Similarly, the intervention of AKT inhibitor showed also the reduced cellular lipid deposition and the upregulated levels of ΔΨm, CPT1 or GSTK1, while the levels of p-AKT and caspase-1 downregulated. Conclusion Arsenic induced lipid deposition in HepG-2 cells is associated with AKT signaling, and APN can antagonize arsenic-induced lipid metabolism disorder and lipid deposition in hepatocytes via inhibiting AKT signaling.
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