D-四氢掌叶防己碱通过AMPK信号通路抑制HepG2肝癌细胞脂肪蓄积的作用及其机制

目的]探讨D-四氢掌叶防己碱在HepG2肝癌细胞中对脂肪蓄积的抑制作用及相关机制．方法]用D-四氢掌叶防己碱（0，5，10，20，40，80umo／L）处理HepG2肝癌细胞24h，采用MTS法测定细咆毒性；采用Westernblot方法检测与脂肪积蓄有关的AMPK蛋白质的表达情况；采用RT-PCR方法检测与AMPK信号通路有关的SREBP1c、脂肪酸舍酶（FAS）及硬脂酰辅酶去饱和酶（SCDl）等相关基因的表达情况．结果]D-四氢掌叶防己碱呈浓度依赖性地抑制三酰甘油的含量，增加AMPK磷酸化；D-四氢掌叶防己碱抑制与脂肪合成有关的SREBPlc、FAS及SCDl基因的表达．结论]D-四氢掌叶防己碱在HepG2肝癌细咆中通过AMPK信号通路抑制脂肪蓄积．

Effects and its mechanism of D-tetrahydropalmatine on attenuating lipid accumulation in HepG2 human hepatoma cells via AMPK signal pathway

OBJECTIVE To study the inhibitory effects and its related mechanism of D-tetrahydropalmatine on lipid accumulation in HepG2 cells. METHODS HepG2 cells were treated with D-tetrahydropalmatine （0, 5, 10, 20 and 40 μmol/L） for 24 h. The cell toxicity of the HepG2 cells were detected by MTS, and the expressions of AMPK was mesured by Western blot, and the expressions of signaling pathway related genes such as SREBPlc, FAS and SCD1 were detected by RT-PCR. RESULTS D-tetrahydropalmatine dose-dependently inhibited the contents of triglyceride, and increased the phosphorylations of AMPK, and inhibited the expressions of lipogenesis gene （SREBPlc, FAS, SCD1）. CONCLUSION D-tetrahydropalmatine inhibits hepatic lipid accumulation in HepG2 human hepatoma cells via AMPK signal pathway.