柴胡皂苷d通过调控lncMEG3抗肝纤维化的机制研究OA

Objective To observe the effect of saikosaponin-d(SSd)on the expression of long noncoding RNA MEG3(ln-cRNA MEG3)in animal and cell models of liver fibrosis,and to explore the effect and mechanism of SSd on liver fibrosis.Meth-ods The expression of lncRNA MEG3 in liver tissue of rats with liver fibrosis induced by carbon tetrachloride(CCl4)was measured using qPCR.A lentiviral vector for interfering with lncMEG3 was constructed.The liver tissue was collected,and the pathological changes of liver fibrosis were examined using Masson and Sirius red staining.Adenovirus-mediated overexpression of lncMEG3 was transfected into TGF-β-induced LX-2 cells,and the effects of lncMEG3 overexpression on the expression levels of fibrotic phenotype α-smooth muscle actin(α-SMA)and collagen-related protein Collagen I were assessed via Western blot and qPCR.qPCR was used to detect the expression changes of lncMEG3 in primary hepatic stellate cells(HSCs)induced by CCl4 and LX-2 cells induced by transforming growth factor-β(TGF-β)treated with SSd.Results Compared with that in the control group,the expression of lncMEG3 was significantly down-regulated in the CCl4 induced liver fibrosis rat model,the extracted pri-mary hepatic stellate cells(HSCs)and TGF induced LX-2 cells.However,the treatment with SSd resulted in partial recovery of lncMEG3 expression.Compared with that in the control group,overexpression of lncMEG3 resulted in the down-regulation of the expressions of Collagen I and α-SMA protein as well as the mRNA expression levels of Collagen Ⅰ and α-SMA.SSd treatment significantly alleviated CCl4 induced liver fibrosis.After inhibiting lncMEG3 with a lentivirus that interferes with lncMEG3,the an-ti fibrotic effect of SSd was weakened.Conclusion SSd can inhibit collagen synthesis and anti liver fibrosis,and its mechanism may be related to the up-regulation of lncRNA MEG3 expression.