Dexamethasone-induced apoptosis in PC12 cells

AbstractThis study aims to evaluate the cytotoxicity and damage of dexamethasone (DEX) on rat pheochromocytoma (PC12) cells by determining cell viability, Hoechst 33342 staining, mitochondrial depolarization assays, opened mitochondrial permeability transition pores (MPTPs) detection, and measurement of Caspase-3 and Bcl-2 activities. The results show that DEX inhibits PC12 cell growth and decreases their viability in a remarkable dose-dependent manner. Our results also reveal that DEX exposure causes morphologic changes, opening of MPTPs and mitochondrial depolarization, upregulates Caspase-3 expression, and suppresses Bcl-2 expression in PC12 cells. These results suggest that DEX-induced apoptosis may be mediated through mitochondrial dysfunction.