芥子酸缓解油酸诱导的HepG2细胞脂毒性凋亡的作用研究

Objective To investigate the effect and mechanism of sinapic acid (SA) on the lipoapoptosis of HepG2 hepatocytes, induced by oleic acid (OA). Methods HepG2 hepatocytes were treated with OA at concentrations of 0, 0.1, 0.3, 0.5, 0.7, 0.9 mmol/L for 24 h. The cell proliferation rate, cytotoEstablishment of a Model of Lipotoxic Injury Induced by Oleate in HepG2 cellsxicity and apoptosis were determined to establish a lipoapoptosis model. Simultaneously, the non-toxic concentration of SA was determined by cck-8 method. 10, 100, 300, 500 μmol/L SA were added into the lipoapoptosis model respectively. Cell proliferation, cytotoxicity, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) and the cell cycle in the cells were determined by the kits. Apoptosis was observed by Hoechst 33342 staining and quantified by Flow Cytometry. The expression of the apoptosis-related gene p53, Bax, caspase-3, caspase-9, and the anti-apoptotic gene Bcl-2 were detected by RT-PCR. Results The lipid apoptosis model was established with 0.7 mmol/L OA for 24 h. Compared with the model group, the addition of 300 μmol/L SA reduced MDA content, increased SOD activity, accelerated cell cycle, and significantly decreased apoptosis rate (p < 0.05). Also, it significantly reduced the high expression of Bax, p53, caspase-3 caused by OA (p < 0.05), while increasing the expression of Bcl-2, and had no significant effect on the expression of caspase-9 gene (p > 0.05). Conclusion SA can resist the lipoapoptosis of HepG2 cells induced by caspase pathway by decreasing the level of oxidative stress induced by OA.