雷公藤红素对神经胶质瘤U87细胞增殖、凋亡和迁移的影响

目的研究雷公藤红素对神经胶质瘤U87细胞增殖、凋亡和迁移的影响及其机制。方法采用MTT法检测雷公藤红素对U87细胞增殖的影响;流式细胞术检测U87细胞凋亡和线粒体膜电位;Western blotting法检测U87细胞中线粒体途径相关凋亡蛋白表达水平;Transwell和划痕实验检测U87细胞的迁移能力。结果雷公藤红素可显著抑制U87细胞的增殖、降低U87细胞线粒体膜电位并诱导U87细胞凋亡;雷公藤红素显著性地调控Bcl-2、Bax、细胞色素C(Cyt C)、Caspase-9和Caspase-3的表达水平;同时雷公藤红素显著抑制U87细胞迁移能力。结论雷公藤红素抑制U87细胞增殖、迁移和诱导其凋亡,其中凋亡机制可能是通过调控线粒体途径相关凋亡蛋白来实现的。

Effects of celastrol on proliferation, apoptosis, and migration of glioma U87 cells

Objective To study the effects of celastrol on the proliferation, apoptosis and migration of human Glioma U87 cells and investigate its preliminary action mechanism. Methods MTT assay were used to evaluate the effects of celastrol on U87 cells proliferation, and flow cytometry were performed to detect U87 cells apoptosis and mitochondrial membrane potential. Expression of apoptosis related proteins in mitochondria pathway were detected by western blotting. Transwell migration assay and wound healing assay were used to study the migration ability of U87 cells. Results After treatment with different concentrations of celastrol, the proliferation of U87 cells was significantly inhibited. The flow cytometry assay showed that celastrol decreased the mitochondrial membrane potential and induced the apoptosis of U87 cells. The mechanism of apoptosis showed that celastrol could significantly regulate the expression levels of Bcl-2, Bax, cytochrome C, caspase-9, and caspase-3 in mitochondria pathway. Additionally, celastrol significantly inhibited the migration of U87 cells. Conclusion Celastrol significantly inhibited the proliferation and migration, and induced apoptosis of U87 cells, which may be mediated by the regulation of mitochondrial pathway related apoptosis proteins.