MicroRNA-181a knockdown protects HepaRG cells from Dichlorvos-induced oxidative stress and apoptosis

The present study was designed to assess the molecular mechanism of Dichlorvos (DDVP)-induced hepatic cell toxicity in vitro using HepaRG cells. The cytotoxicity was determined by cell viability, apoptosis portion, and reactive oxygenspecies (ROS) generation. The results indicated that DDVP treatment significantly inhibited cell growth, induced cell apoptosis and promoted the production of ROS on HepaRG cells. Microarray analysis showed that miR-181a was significantly upregulated in HepaRG cells treated with DDVP. Furthermore, we found that miR-181a downregulation has a remedy effect on DDVP-induced cell toxicity, while miR-181a overexpression augments the DDVP-induced hepatic cell apoptosis and ROS production. Furthermore studies showed that miR-181a directly targeted Bcl-2, and Bcl-2 downregulation inhibited the remedy effect of miR-181a inhibitor on DDVP induced cell toxicity. It is, therefore, concluded that miR-181a knockdown could protect hepatic cells from DDVP induced oxidative stress and apoptosis by targeting bcl-2.