Acrylamide induces apoptosis via ERS and autophagy
1. Department of Health Toxicology,MOE Key Lab of Environment and Health,School of Public Health,Tongji Medical College,Huazhong University of Science and Technology2. Experimental Teaching Center of PreventiveMedicineSchool of PublicHealth,TongjiMedical College,Huazhong University of Science & Technology
摘要：Acrylamide（ACR） has obvious neurotoxicity in human by causing apoptosis, endoplasmic reticulum stress, and autophagy, but the relationships among were still unclear. This study aimed to investigate the roles of ERS and autophagy in vitro, to further demonstrate the mechanism of ACR neurotoxicity. In present study, different doses of ACR were set, to value ACR toxicity, then the PERK inhibitor and autophagy inhibitor, GSK2606414 and 3-Methyladenine, were used separately to inhibit ERS and autophagy activation under ACR treatment. With the increases of ACR dose, the cell viability and apoptotic rate dose-dependently decreased. After ERS inhibition, the apoptosis and autophagy caused by ACR were alleviated, showing reduced apoptotic rate, and down-regulated levels of Bax, Beclin1, LC3-Ⅱ/LC3-Ⅰ. While the autophagy inhibition deteriorated apoptosis, with up-regulated apoptotic rate, and increased Bax, indicating ACR caused autophagy by activating PERK pathway of ERS, and induced apoptosis finally. This study helps to provide experimental basis for exploring potential molecular targets for the prevention and control of ACR toxicity.