Subjects: Medicine, Pharmacy >> Preventive Medicine and Hygienics submitted time 2024-04-01
Abstract： Objective To explore the intervention effect of Lentinan (LNT) on liver lipid deposition induced by sodium arsenite (SA) in C57BL/6 mice. Methods The experiment was divided into four groups (8 mice/group): control group, SA exposure group, LNT intervention+SA exposure group, LNT control group. C57BL/6 mice were exposed by SA (SA dissolved in deionized water, drinking water exposure 10.0 mg/L, 8 weeks) and LNT intervention treatment (1.0 mg/kg, intramuscular injection, once every other day, 8 weeks). After the experiment, liver tissue samples were collected and the characteristics of liver lipid deposition were observed by oil red O staining of liver tissue sections. The levels of triglyceride (TG) and adiponectin (APN) in the liver tissue of mice were detected by enzyme-linked immunosorbent assay (ELISA), and the statistical differences between the groups were analyzed by analysis of variance (ANOVA) and least significant difference (LSD). Results Compared with control group, SA exposure mice showed that lipid deposition in liver tissues, decreased APN level, and increased TG level (P<0.05). Compared with SA exposure group, LNT intervention+SA exposure group showed that the reduced degree of liver lipid deposition, the increased level of APN, and the decreased level of TG (P<0.05). For LNT control group, similar to the control group, the liver tissue morphology was normal, and the levels of APN and TG had no statistical difference compared with the control group (P>0.05). Conclusion SA-induced liver lipid deposition in C57BL/6 mice may be related to the down-regulation of APN level. LNT intervention can increase APN level to antagonize SA-induced liver lipid deposition in C57BL/6 mice.
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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