Sodium aescinate induces apoptosis of HeLa cells by inhibiting Akt/ERK signaling pathways and increasing death receptor expression

AIM:To study the effects of sodium aescinate on the apoptosis of cervical cancer HeLa cells and its molecular mechanism. METHODS:MTT assay was used to detect the growth and proliferation of HeLa cells. The morphological alteration was observed under inverted microscope. Annexin V-FITC/PI double staining and DAPI nuclear staining were used to determine the apoptosis of HeLa cells induced by sodium aescinate. The apoptosis-related proteins PARP, cleaved caspase-8 and pro-caspase-3, and the proliferation-associated molecules Akt and ERK, as well as TRAIL receptors DR4 and DR5 were detected by Western blotting. RESULTS:Sodium aescinate inhibited the growth of HeLa cells in a concentration-dependent manner. Treatment with sodium aescinate induced the typical morphology of apoptotic cells and increased the apoptotic rate significantly. The cleaved PARP, cleaved caspase-8 and cleaved caspase-9 protein expression was observed. The expression of DR4 and DR5 was up-regulated. Meanwhile, pro-caspase-3 was decreased, and the levels of p-Akt and p-ERK were down-regulated by sodium aescinate in a dose-dependent manner. CONCLUSION:Sodium aescinate inhibits the proliferation and promotes the apoptosis of HeLa cells by increasing death receptor expression and repressing proliferation-associated signaling pathways.