LncRNA SRA在游离脂肪酸诱导的LO2细胞脂肪蓄积中的作用

Role of Lnc RNA SRA in free fatty acid-induced lipid accumulation in LO2 cells

目的通过游离脂肪酸(FFA)刺激LO2细胞来观察肝细胞脂肪蓄积的情况和长非编码RNA类固醇受体RNA激活剂(Lnc RNA SRA)在其中的调控机制。方法体外培养人肝癌细胞系LO2细胞,采用不同浓度的棕榈酸(PA)(0、0.2、0.4、0.8 mmol/L PA)处理细胞。采用油红O染色检测LO2细胞内脂肪蓄积情况;q PCR和Western blot分别测定细胞内基因和蛋白表达情况。结果 0.2 mmol/L的PA刺激能使LO2细胞发生脂肪蓄积。与对照组比较,PA组LO2细胞Lnc RNA SRA的表达异常升高(P<0.05),脂肪甘油三酯脂酶(ATGL)和叉头框蛋白O1(Fox O1)的表达明显降低,差异有统计学意义(P<0.05)。结论游离脂肪酸可以导致LO2细胞脂肪蓄积性损伤,可能是通过Lnc RNA SRA抑制ATGL的表达,进而降低脂质氧化的途径完成的。

Objective To observe the effects and Lnc RNA SRA mechanism of free fat acid induced lipidosis in LO2 cells.Methods LO2 cells were cultured in vitro. The control group and palmic acid（PA）groups（0.2 mmol/L）were established according to the experimental requirements. The lipidosis was measured by Oil Red O staining. The m RNA and protein expression levels were determined by q PCR and Western-blot,respectively. Results Compared with control group,0.2 mmol/L PA treatment could induce lipidosis. Meanwhile,PA group had higher levels of Lnc RNA SRA（P〈0.05）,lower levels of adipose triglyceride lipase（ATGL）（P〈0.05）and Forkhead box protein O1（FoxO1）m RNA expression level（P〈0.05）. Conclusion Lnc RNA SRA promotes free fat acid induced hepatic steatosis through repressing the expression of ATGL in LO2 cells.