Internet Archive Scholar

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

Caifeng Gu, Jie Shen, Feng Zhang, Junfeng Chen
2017 Int J Clin Exp Pathol   unpublished

Preserved Fulltext

fulltext thumbnail
Web Archive Capture PDF (1.3 MB)
https://web.archive.org/web/20180421103834/http://www.ijcep.com/files/ijcep0057142.pdf

A copy of this work was available on the public web and has been preserved in the Wayback Machine. The capture dates from 2018; you can also visit the original URL. The file type is application/pdf.

The present study was designed to assess the molecular mechanism of Dichlorvos (DDVP)-induced he-patic 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
more » ... s 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 oxida-tive stress and apoptosis by targeting bcl-2.
fatcat:cc5tb6eoebbutmqiifmmfkp7e4
Citation

Caifeng Gu, Jie Shen, Feng Zhang, Junfeng Chen. "Original Article MicroRNA-181a knockdown protects HepaRG cells from Dichlorvos-induced oxidative stress and apoptosis." Int J Clin Exp Pathol 10.11 (2017)