Remifentanil induces autophagy and prevents hydrogen peroxide-induced apoptosis in Cos-7 cells.
10.17245/jdapm.2016.16.3.175
- Author:
Ji Young YOON
1
;
Chul Woo BAEK
;
Mi Na WOO
;
Eun Jung KIM
;
Ji Uk YOON
;
Chang Hoon PARK
Author Information
1. Department of Dental Anesthesia and Pain Medicine, Pusan National University Dental Hospital, Yangsan, Korea. wjdental@hanmail.net
- Publication Type:Original Article
- Keywords:
Apoptosis;
Autophagy;
Cos-7 cells;
Oxidative stress;
Remifentanil
- MeSH:
Animals;
Apoptosis*;
Autophagy*;
Blotting, Western;
Cell Death;
Cell Survival;
COS Cells*;
Hydrogen*;
Microscopy, Fluorescence;
Oxidative Stress;
Survival Rate
- From:Journal of Dental Anesthesia and Pain Medicine
2016;16(3):175-184
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: This study investigated the effect of remifentanil pretreatment on Cos-7 cells exposed to oxidative stress, and the influence of remifentanil on intracellular autophagy and apoptotic cell death. METHODS: Cells were divided into 4 groups: (1) Control: non-pretreated cells were incubated in normoxia (5% CO₂, 21% O₂, and 74% N₂). (2) H₂O₂: non-pretreated cells were exposed to H₂O₂ for 24 h. (3) RPC+H₂O₂: cells pretreated with remifentanil were exposed to H₂O₂ for 24 h. (4) 3-MA+RPC+H₂O₂: cells pretreated with 3-Methyladenine (3-MA) and remifentanil were exposed to H₂O₂ for 24 h. We determined the cell viability of each group using an MTT assay. Hoechst staining and FACS analysis of Cos-7 cells were performed to observe the effect of remifentanil on apoptosis. Autophagy activation was determined by fluorescence microscopy, MDC staining, and AO staining. The expression of autophagy-related proteins was observed using western blotting. RESULTS: Remifentanil pretreatment increased the viability of Cos-7 cells exposed to oxidative stress. Hoechst staining and FACS analysis revealed that oxidative stress-dependent apoptosis was suppressed by the pretreatment. Additionally, fluorescence microscopy showed that remifentanil pretreatment led to autophagy-induction in Cos-7 cells, and the expression of autophagy-related proteins was increased in the RPC+H₂O₂ group. CONCLUSIONS: The study showed that remifentanil pretreatment stimulated autophagy and increased viability in an oxidative stress model of Cos-7 cells. Therefore, we suggest that apoptosis was activated upon oxidative stress, and remifentanil preconditioning increased the survival rate of the cells by activating autophagy.
