矢车菊素-3-葡萄糖苷诱导Hela细胞凋亡及其机制的研究

目的研究花色素苷与矢车菊素-3-葡萄糖苷对人宫颈癌细胞株Hela细胞体外增殖作用并从细胞学和分子生物学水平探讨其作用机制。方法从黑米中提取出花色素苷,再分离出矢车菊素-3-葡萄糖苷单体;用不同浓度的花色素苷和矢车菊素-3-葡萄糖苷分别处理Hela细胞后,CCK-8法测细胞生长抑制率;Hoechst 33258染色,激光共聚焦镜下观察细胞形态;流式细胞仪检测凋亡率;SABC染色检测Bax/Bcl-2的蛋白表达。结果25~400 mg/L花色素苷和12.5~200μmol/L矢车菊素可抑制Hela细胞生长,抑制率呈时间剂量依赖性;激光共聚焦镜下可见到明显的凋亡细胞;流式细胞仪检测药物处理后出现明显凋亡率;药物可使Bax表达上调,Bcl-2表达下降。结论花色素苷与矢车菊素-3-葡萄糖苷都可抑制Hela细胞生长,诱导其凋亡,其诱导凋亡的作用的机制与凋亡相关基因促凋亡基因Bax表达上调,抗凋亡基因Bcl-2表达下调有关。

The studies of cyanidin 3-glucoside-induced apoptosis in human cervical cancer Hela cells and its mechanism

Purpose To investigate the regulatory effect of anthocyanin and cyanidin 3-glucoside on proliferation and apoptosis in human cervical carcinoma cell line Hcla in vitro and its possible mechanism at cellular and molecular levels.Methods Hela cells were treated with black rice anthocyanin(BA)and cyanidin 3-glucoside(C3G)at various concentrations for different durations.The growth inhibition rates of Hela cells were determined by CCK-8.Cell apoptosis was inspected by laser scanning confocal microscope(LSM).Flow cytometry(FCM)was applied to measure the apoptotic rate.In addition,the expression of Bax/Bcl-2 protein in Hela cell was observed by SABC immunohistochemistry.Results BA and C3G inhibited the proliferation of Hela cells in a dose-and time-dependent manner.Partial cells presented the characteristic morphological changes of apoptosis under the electron Microscope.The apoptotic rates were significantly raised in FCM.The Bax expression was increased while Bcl-2 expression was decreased.Conclusion BA and C3G could significantly inhibit the growth of Hela cells,inducing apoptosis via regulating the expressions of Bax.Bcl-2 is probably one of its molecular mechanisms.