Dehydroepiandrosterone rehabilitate BRL ‐3A cells oxidative stress damage induced by hydrogen peroxide

This study aimed to investigate the molecular mechanism of dehydroepiandrosterone (DHEA) rehabilitated BRL‐3A cells oxidative stress damage induced by hydrogen peroxide (H2O2). Results showed that DHEA reversed the decrease of cell viability and ameliorated nuclear chromatin damage in H2O2‐induced BRL‐3A cells. DHEA increased the activities of superoxide dismutase, catalase, peroxidase, and glutathione peroxidase, and decreased the reactive oxygen species (ROS) production in H2O2‐induced BRL‐3A cells. DHEA attenuated the protein damage and lipid peroxidation, and reduced the apoptosis in H2O2‐induced BRL‐3A cells. The mRNA levels of Bax, Caspase‐9, and Caspase‐3 were decreased, while the Bcl‐2 mRNA level was increased in H2O2‐induced BRL‐3A cells treated with DHEA. Our results showed that DHEA treatment increased the PI3K and p‐Akt protein levels, while decreased the Bax and capase‐3 protein levels in H2O2‐induced BRL‐3A cells. However, the rise in PI3K and p‐Akt protein levels, and the decrease in Bax and capase‐3 protein levels induced by DHEA treatment were reversed when the cells pretreated with LY294002 (PI3K inhibitor). These results indicated that DHEA ameliorated H2O2‐induced oxidative damage by increasing anti‐oxidative enzyme activities and ameliorating the protein damage and lipid peroxidation in BRL‐3A cells. In addition, DHEA decreased the apoptosis by inhibiting caspase‐3 and Bax protein levels and this action mainly a...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research