Delayed cardioprotection by sevoflurane preconditioning: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury.
机构：[1]Department of Anesthesiology, Second Affiliated Hospital of Soochow University, Suzhou 215004, China[2]Department of Anesthesiology, Second Affiliated Hospital to Nanchang University, Nanchang 330006, China[3]Department of Anesthesiology and Critical Care, Second Affiliated Hospital of Soochow University, Suzhou 215004, China.
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摘要：
Sevoflurane preconditioning has shown to exert delayed caridioprotection against subsequent ischemia and reperfusion injury, but the mechanisms underlying is unclear. Inhibition of autophagy by 3-methyladenine (3-MA) or knockdown of Beclin 1 leads to enhanced cardiac myocyte survival. Our study aimed to test whether sevoflurane preconditioning provides a second window of anesthetic preconditioning (SWOP) via inhibit Beclin 1-mediated autophagic cell death. H9c2 rat cardiomyocytes were randomly divided into five groups: Control (CON) group; hypoxia/reoxygenation (H/R) group, rat cardiomyocytes was exposed in the airtight container for 2 h followed by 1 h of reoxgenation; SWOP group, rat cardiomyocytes was exposed to 1 h of 2.5% sevoflurane 24 h before H/R; Autophagic inhibitors, 3-methyladenine (3-MA, 10 mM) was added to culture medium 15 min before sevoflurane exposure (3-MA+SWOP group) or cells were treated by 3-MA alone (3-MA group). The cell proliferation was significantly increased in SWOP group (79.49 ± 1.37%, P < 0.05) when compared to H/R group (62.2 ± 6.49%, P < 0.05). 3-MA administered before SWOP significantly attenuated the H/R induced autophagy and cell death. H/R injury up-regulated the expression of LC3-II and Beclin 1 proteins (342 ± 66% and 163 ± 18%, respectively, P < 0.05) compared to the CON group (100%), which were increased in SWOP group (202 ± 77% and 128 ± 8%, respectively, P < 0.05). The expression of LC3-II and Beclin 1 proteins was decreased in 3-MA group (110 ± 28% and 97 ± 6%, respectively) and 3-MA+SWOP group (93 ± 7% and 98 ± 6%, respectively) compared with H/R group, but Bcl-2 was upregulated in 3-MA group (158 ± 4%) and 3-MA+SWOP group (156 ± 5%) compared to H/R group (103 ± 7%). In conclusion, sevoflurane preconditioning confers delayed cardioprotection via inhibition Beclin 1-mediated autophagic cell death in cardiac myocytes 24 h before exposed to H/R injury.
基金：
This work was supported by grants No. BK20141187 (to Dr. Wang) from the Natural Science Foundation of Jiangsu Province, and by Grants No SYS201473 (to Dr. Qiao) from the Technology Bureau of Suzhou, China. Dr. Wang also received support from the Project of Gusu Health Key Talent. The Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions.
第一作者机构：[1]Department of Anesthesiology, Second Affiliated Hospital of Soochow University, Suzhou 215004, China
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通讯机构：[*1]Departments of Anesthesiology and Critical Care, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou 215004, China.
推荐引用方式(GB/T 7714)：
Hong Xie,Qin Liu,Shigang Qiao,et al.Delayed cardioprotection by sevoflurane preconditioning: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury.[J].International journal of clinical and experimental pathology.2015,8(1):217-26.
APA：
Hong Xie,Qin Liu,Shigang Qiao,Xiuli Jiang&Chen Wang.(2015).Delayed cardioprotection by sevoflurane preconditioning: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury..International journal of clinical and experimental pathology,8,(1)
MLA：
Hong Xie,et al."Delayed cardioprotection by sevoflurane preconditioning: a novel mechanism via inhibiting Beclin 1-mediated autophagic cell death in cardiac myocytes exposed to hypoxia/reoxygenation injury.".International journal of clinical and experimental pathology 8..1(2015):217-26
