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目的:应用体外培养骨髓基质细胞,在细胞和分子水平观察补骨合剂对细胞凋亡的影响,探讨补骨合剂治疗骨质疏松症的机制。方法:分离SD大鼠骨髓基质细胞,通过形态学方法和流式细胞术检测凋亡细胞周期和线粒体膜电位改变以及Bcl-2、Bax蛋白基因表达,对补骨合剂在细胞凋亡过程中的作用进行评价。结果:补骨合剂的早期应用可以使阻滞于G0/G1期的细胞减少,进入S期进行DNA合成的细胞增多;诱导凋亡的细胞在补骨合剂组Bcl-2表达明显高于全反式维甲酸(all-transretinoicacid,ATRA)诱导组,而Bax表达明显低于ATRA诱导组,且补骨合剂组线粒体的膜电位下降均显著低于ATRA诱导组。结论:补骨合剂治疗骨质疏松症的机制是补骨合剂的早期应用可以使ATRA诱导的凋亡细胞减少,从而促进细胞有丝分裂,抑制细胞凋亡;对骨髓基质细胞线粒体膜上的Bcl-2具有保护作用,同时通过阻止Bax从胞浆中移至线粒体膜上而使Bcl-2在与Bax形成的同源二聚体中占据优势来阻止线粒体膜上的通透性转换孔道开放,从而阻止线粒体释放凋亡诱导因子造成的线粒体膜电位改变和生物合成的破坏,达到抑制凋亡的目的。
OBJECTIVE: To observe the effect of Bugu Mixture on cell apoptosis in vitro by culturing bone marrow stromal cells and explore the mechanism of Bugu Mixture in treating osteoporosis. Methods: Bone marrow stromal cells were isolated from SD rats. Morphological and flow cytometry were used to detect the changes of cell cycle and mitochondrial membrane potential as well as the gene expression of Bcl-2 and Bax. The effects of Bugu Mixture on apoptosis Evaluation of the role. Results: The early application of Bugu Mixture can reduce the number of cells arrested in G0 / G1 phase and the number of cells entering DNA synthesis phase in S phase. The expression of Bcl-2 in Bugu Mixture group was significantly higher Induced by all-transretinoic acid (ATRA), but the expression of Bax in ATRA-induced group was significantly lower than that in ATRA-induced group. The mitochondrial membrane potential of BuBu combination group was significantly lower than that of ATRA-induced group. Conclusion: The mechanism of Bugu Mixture in the treatment of osteoporosis is that the early application of Bugu Mixture can reduce ATRA-induced apoptotic cells, promote cell mitosis and inhibit apoptosis. Bcl-2 on mitochondrial membrane of bone marrow stromal cells Has a protective effect while preventing Bax from predominating in homodimers with Bax by preventing the transfer of Bax from the cytoplasm to the mitochondrial membrane to prevent the permeability transition pore opening on the mitochondrial membrane and thus prevent Mitochondria release of apoptosis-inducing factor caused by mitochondrial membrane potential changes and the destruction of biosynthesis, to inhibit the purpose of apoptosis.