论文部分内容阅读
目的:探讨赤芍总甙(TGC)诱导肿瘤细胞凋亡机制,为TGC的开发应用提供实验依据。方法:采用流式细胞仪测定细胞凋亡,SABC免疫组化法检测Bcl-2蛋白表达,原位杂交法测定c-myc mRNA表达,电镜观察凋亡小体。结果:TGC治疗组出现Ap峰GO-G1期细胞明显减少,S期细胞明显增多,与模型对照组比较有显著差异(P<0.05)。实验组下调相关基因Bcl-2蛋白和c-myc mRNA表达水平。TGC组电镜可见细胞内膜结构完好,染色质边集,细胞核形成核带和核突,凋亡细胞数目较多,有新月形或花环状(凋亡小体形成)。结论:TGC诱导肿瘤细胞凋亡,其机制可能与下调Bcl-2和c-myc mRNA表达水平密切相关。
OBJECTIVE: To investigate the mechanism of apoptosis induced by TGP and provide experimental basis for the development and application of TGC. Methods: Apoptosis was determined by flow cytometry. The expression of Bcl-2 protein was detected by SABC immunohistochemistry. The expression of c-myc mRNA was measured by in situ hybridization. Apoptotic bodies were observed by electron microscopy. RESULTS: In the TGC treatment group, there was a significant decrease in the Ap peak GO-G1 phase cells and a significant increase in S phase cells, which was significantly different from the model control group (P<0.05). The experimental group down-regulated the expression of related genes Bcl-2 protein and c-myc mRNA. The electron microscopy of the TGC group showed that the inner cell membrane structure was intact, the chromatin margin was set, the nucleus formed nuclei and nuclei, the number of apoptotic cells was more, there was a crescent or flower ring (apoptotic body formation). Conclusion: The apoptosis of tumor cells induced by TGC may be related to the down-regulation of Bcl-2 and c-myc mRNA expression.