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

作者：Li, Longlong; Zhao, Jinlong; Ge, Chongyang; Yu, Lei; Ma, Haitian^*

来源：Journal of Cellular Physiology, 2018, 233(8): 6262-6272.

DOI：10.1002/jcp.26458

• BRL-3A cells
• cell apoptosis
• dehydroepiandrosterone
• oxidative damage
• PI3K
• Akt pathways

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 achieved via the activation of PI3K/Akt signaling pathways in H2O2-induced BRL-3A cells. These results provided substantial information for DHEA as a nutritional supplement to treat oxidative stress and it related diseases in animals and humans.

• 出版日期2018-8
• 单位南京农业大学