Remifentanil induces autophagy and prevents hydrogen peroxide-induced apoptosis in Cos-7 cells
À±Áö¿µ, ¹éö¿ì, Woo Mi-Na, ±èÀºÁ¤, À±Áö¿í, ¹ÚâÈÆ,
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À±Áö¿µ ( Yoon Ji-Young ) - Pusan National University Dental Hospital Department of Dental Anesthesia and Pain Medicine
¹éö¿ì ( Baek Chul-Woo ) - Pusan National University Dental Hospital Department of Dental Anesthesia and Pain Medicine
( Woo Mi-Na ) - Pusan National University Dental Hospital Department of Dental Anesthesia and Pain Medicine
±èÀºÁ¤ ( Kim Eun-Jung ) - Pusan National University Dental Hospital Department of Dental Anesthesia and Pain Medicine
À±Áö¿í ( Yoon Ji-Uk ) - Pusan National University Yangsan Hospital Department of Anesthesia and Pain Medicine
¹ÚâÈÆ ( Park Chang-Hoon ) - Pusan National University Dental Hospital Department of Dental Anesthesia and Pain Medicine
KMID : 0980320160160030175
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.
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Apoptosis; Autophagy; Cos-7 cells; Oxidative stress; Remife
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