bcl-2和p53在丹皮酚诱导人结直肠癌HT-29细胞凋亡中的作用及其机制

目的 探讨bcl-2和p53在丹皮酚（paeonol，Pae）诱导入结直肠癌HT-29细胞凋亡过程中的作用及可能的作用机制。方法 应用透射电镜技术和原位末端标记（TUNEL）法观察不同浓度的Pae对HT-29细胞凋亡的诱导作用，应用免疫细胞化学技术检测用药前、后凋亡相关基因bcl-2及p53表达的变化，并与对照组比较。结果 透射电镜观察到Pae作用后HT-29细胞出现典型的细胞凋亡形态；Pae在15．63mg／L、62．50mg／L、250．00mg／L3种浓度下作用48h均可诱导HT-29细胞凋亡，TUNEL法显示各组凋亡指数（AI）间差别有显著性意义（P〈0．05）；免疫细胞化学染色显示Pae作用后HT-29细胞bcl-2及p53蛋白表达显著降低。结论 Pae能抑制HT-29细胞增殖并诱导其凋亡，其作用可能与下调bcl-2及p53蛋白的表达有关。

Effects of bcl -2 and p53 in Paeonol Induced Apoptosis of Human Colorectal Cancer Cell Line HT -29 and the Mechanism

Objective To investigate the effects of bcl-2 and p53 in paeonol(Pae)induced apoptosis of HT-29 cell and their possible molecular mechanism.Methods The induction of apoptosis on HT-29 cells were measured by transmission electron microscopy and TUNEL assay.The expression of apoptosis associated genes bcl-2 and p53 was observed by immunocytochemical staining.Results Typical apoptosis morphology of HT-29 cells was observed by transmission electron microscopy after treated by Pae.Pae could induce apoptosis of HT-29 cells when it was applied at the concentration of 15.63 mg/L,62.50 mg/L and 250.00 mg/L for 48 h.TUNEL assay showed a concentration-effect relationship between Pae and apoptosis index(P<0.05).Immunocytochemical staining showed that the expression of bcl-2 and p53 protein in HT-29 cells was decreased significantly after treated by Pae.Conclusion Pae may inhibit HT-29 cells proliferation and induce its apoptosis.The possible mechanism is down-regulation of the expression of bcl-2 and p53 protein.