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目的探讨PI3K抑制剂(PI103)对肝星状细胞(HSC)PI3K/AKT通路及Ⅲ型胶原表达的影响,为肝纤维化的治疗提供理论基础。方法将液氮保存下的HSC株,于37℃,5%CO2孵育箱中复苏传代培养,同步化后将细胞分为3组:空白对照组、CCl4组、CCl4+PI3K抑制剂组。QPCR方法检测PI3K、AKT信号分子mRNA水平的变化;免疫细胞化学方法测定HSC的PI3K、AKT信号分子和Ⅲ型胶原表达情况。结果 CCl4组和空白对照组比较,PI3K、AKT信号分子mRNA水平和蛋白表达均增多,Ⅲ型胶原生成增多,差异有统计学意义(P<0.05)。CCl4组和CCl4+PI103组比较,PI3K、AKT信号分子mRNA水平和蛋白表达均减少,III型胶原生成减少,差异有统计学意义(P<0.05)。结论 PI3K抑制剂可降低PI3K、AKT信号分子及Ⅲ型胶原的表达,进而阻断肝纤维化进程。
Objective To investigate the effect of PI3K inhibitor (PI103) on the PI3K / AKT pathway and the expression of type Ⅲ collagen in hepatic stellate cells (HSC), and to provide a theoretical basis for the treatment of hepatic fibrosis. Methods HSC strains preserved in liquid nitrogen were resuscitated in 37 ℃, 5% CO2 incubator and subcultured. After synchronization, the cells were divided into three groups: blank control group, CCl4 group and CCl4 + PI3K inhibitor group. QPCR method was used to detect the mRNA level of PI3K and AKT. The expression of PI3K and AKT signal molecules and type Ⅲ collagen in HSC were detected by immunocytochemistry. Results Compared with the blank control group, the mRNA and protein expressions of PI3K and AKT increased and the type Ⅲ collagen production increased. The difference was statistically significant (P <0.05). Compared with CCl4 group and CCl4 + PI103 group, the mRNA and protein expressions of PI3K and AKT decreased, and the type III collagen decreased. The difference was statistically significant (P <0.05). Conclusion PI3K inhibitor can decrease the expression of PI3K and AKT signaling molecules and type Ⅲ collagen, and then block the progression of hepatic fibrosis.