TGF-β2诱导晶状体上皮细胞凋亡的机制

Objective To explore the mechanism of apoptosis of human lens epithelial cells (HLEC) induced by transforming growth factor-β2 (TGF-β2) during the process of posterior capsular opacification (PCO). Methods After treating HLEC with different concentrations of TGF-β2 (0, 0.1, 1, 10 μg/L), the expression of apoptosis-related proteins in the mitochondrial pathway induced by TGF-β2 was detected by Western blot; the specific form of cell apoptosis induced by 5 μg/L TGF-β2 and the effect of treating cells with 5 μg/L TGF-β2 for 36 hours on the cell cycle were detected by flow cytometry. Results TGF-β2 could significantly increase the expression of Caspase 3 (P<0.001), the expression ratio of the pro-apoptotic protein Bax to the anti-apoptotic protein Bcl-2 was imbalanced (P<0.001) and was concentration-dependent, activating the apoptosis of the Bax/Bcl-2 - caspase3 pathway in the endogenous mitochondrial pathway. 5 μg/L of TGF-β2 could induce apoptosis of HLEC (P<0.05), and after treating the cells for 36 hours, it could cause G1/S cycle arrest. Conclusion During the process of PCO, cell apoptosis in the mitochondrial pathway induced by TGF-β2 is accompanied, which may be involved in the formation process of PCO and will provide new ideas for the pathogenesis of PCO and drug development.

目的探讨晶状体后囊膜混浊(posterior capsular opacification, PCO)过程中转化生长因子-β2(transforming growth factor β2, TGF-β2)诱导晶状体上皮细胞(human lens epithelial cell, HLEC)凋亡的机制。方法用不同浓度TGF-β2(0、0.1、1、10 μg/L)处理HLEC后,Western blot检测TGF-β2诱导的线粒体途径依赖的细胞凋亡相关蛋白表达;流式细胞仪检测5 μg/L TGF-β2诱导细胞凋亡的具体形式,以及5 μg/L TGF-β2处理细胞36 h对细胞周期的影响。结果TGF-β2可明显增加Caspase3的表达(P<0.001),促凋亡蛋白Bax与抑凋亡蛋白Bcl-2的表达比例失调(P<0.001)并呈浓度依赖性,激活内源性线粒体途径的Bax/Bcl-2-caspase3通路的凋亡。5 μg/L的TGF-β2可以诱导HLEC发生凋亡(P<0.05),处理细胞36 h后可导致G1/S周期阻滞。结论PCO过程中伴随TGF-β2诱导的线粒体途经的细胞凋亡,可能参与了PCO的形成过程,将为PCO发病机理及药物开发提供新思路。