Role of Akt/HIF-1α Signaling Pathway in PC12 Cell Injury Induced by Selenium Dioxide

Abstract: This article was to investigate the role of Akt/HIF-1α (hypoxia inducible factor-1α) signaling pathway in the injury of PC12 cells induced by selenium dioxide (SeO2) in rat adrenal pheochromocytoma. PC12 cells were exposed to different concentrations of SeO2 (40， 80， 160 μmol/L) for 24 h to induce cell injury. The cell viability was measured by MTT assay. Morphological changes of cells were observed by inverted microscope. The degree of cell injury was measured by lactate dehydrogenase leakage detection. The intracellular production of reactive oxygen species (ROS) was measured by assessing superoxide dismutase (SOD) and malonic dialdehyde (MDA) levels， cell apoptosis was determined by Hoechst 33342 staining， and the levels of HIF-1α， p-Akt， Bcl- 2， Bax， PI3k， p53 and Caspase-3 were determined by Western blot. Selenium dioxide could induce the damage of PC12 cells in a dose-dependent manner， and potentiated oxygen radical production and cell apoptosis， causing cell shrinkage and axonal shortening. The levels of p-Akt， HIF-1α， p53， Caspase-3 (cysteinyl aspartate specific proteinase-3) were up-regulated and the ratio of Bax/Bcl-2 expression was significantly increased by selenium dioxide in PC12 cells. These results indicated that the damage of PC12 cells causing cell apoptosis was induced by selenium dioxide， which was related to the activation of Akt/HIF-1α signaling pathway and the expression of p53， Bax/Bcl-2， Caspase-3 and intracellular free radicals.

CSTR: 32200.14.cjcb.2017.11.0007