黄连素通过提高活性氧水平促进HepG2细胞凋亡

Berberine induces apoptosis in HepG-2 initiated by reactive oxygen species

本研究用SRB法、流式细胞术和荧光显微技术等方法检测分析了黄连素对人肝癌细胞株HepG-2的毒性并探究了其作用机制.结果显示,黄连素的毒性作用呈时间-剂量依赖效应,24h和48h的IC50值分别为44.10μmol·L^(-1)和8.53μmol·L^(-1);160μmol·L^(-1)时黄连素具有致死效应;当加入抗氧化剂NAC,黄莲素抑制和致死作用明显减弱.黄连素可引起HepG-2细胞凋亡,NAC作用后细胞凋亡率降低;黄连素可使胞内ROS含量持续升高;同时在黄连素作用下还降低了细胞内抗氧化剂GSH含量.表明黄连素可以通过提高细胞内ROS,耗竭胞内抗氧化剂进而诱导肝癌细胞凋亡.

The current study aims to detect the cytotoxicity and diScuss mechanism of berberine to humanhepatoma cells with the method of SRB, flow cytometry and fluorescence microscope. The results showthat berberine exhibited time and dose--dependent antiproliferative effects in hematoma cells HepG-2.ICs0 were 44.10 mol- L-1 and 8.53 μmol- L 1 when treated 24 h and 48 h respectively, but cell deathappeared when 160μmol. L-1 berberine were used. The antiproliferation and death could be blocked in thepresence of antioxidant N-acetylcysteine（NAC）. And, our find that berberine -- mediated apoptosis inhuman hepatoma cell through inducing reactive oxygen species producing and depleted GSH. Therefore,we suggests that berberine may be considered for further studies as a promising therapeutic candidate forhepatic caucinoma.