基于肝癌细胞线粒体功能受损和 caspase-3 信号通路 探讨罗哌卡因促进肝癌细胞凋亡的作用机制研究.

Objective: To explore the mechanism of ropivacaine promoting apoptosis of hepatoma carcinoma cell based on mitochondrial dysfunction and caspase-3 signaling pathway. Methods: Human hepatoma carcinoma cell line BEL-7402 was used for experimental study. After Bel-7402 cells were treated with different concentrations of ropivacaine, the proliferation of hepatoma carcinoma cell was detected by MTT method, the cell morphology was observed by light microscopy and DAPI solution staining, the cell viability was determined by trypan blue staining, the apoptosis of Bel-7402 cells was analyzed by flow cytometry, and the mitochondria were observed under electron microscopy. The nuclear migration of caspase-3 in Bel-7402 cells was observed by laser confocal microscopy, and the effects of ropivacaine on the expression of cytoplasmic apoptosis-related proteins, mitochondrial apoptosis-related proteins, Bel-7402 cells and mitochondrial apoptosis-related proteins were evaluated by western blot assay. Results: Ropivacaine can inhibit the growth of hepatoma carcinoma cell in a dose-dependent and time-dependent manner. The apoptosis of Bel-7402 cells was induced by ropivacaine, and the apoptosis rate of Bel-7402 cells was significantly increased. Ropivacaine can injure mitochondrial function of hepatoma carcinoma cells. Laser confocal microscopy showed the migration of caspase-3 molecules to the nucleus. Ropivacaine interacts with caspase-3 to promote the migration of caspase-3 into the nucleus, stimulate the expression of caspase-3, PARP-1 and caspase-9 proteins, inhibit the expression of Bcl-2, promote the expression of APAF-1, promote mitochondria to release Cytochrome C and activate caspase-3 activity. Conclusion: Ropivacaine can promote the apoptosis of hepatoma carcinoma cell, and its mechanism may be related to the destruction of mitochondrial function and activation of caspase-3 signaling pathway. [ABSTRACT FROM AUTHOR]