Effect of sevoflurane postconditioning on microtubule structure during myocardial ischemia-reperfusion in mice
Hai Guo, Min Zheng, Pan Zhao, Haiping Ma, Hong Zheng
Abstract
Hai Guo, Min Zheng, Pan Zhao, Haiping Ma, Hong Zheng
Abstract
Objective To evaluate the effect of sevoflurane postconditioning on microtubule structure during myocardial ischemia-reperfusion (I/R) in mice. Methods Thirty-two healthy male C57 mice, aged 7-8 weeks, wighing 20-30 g, were divided into 4 groups (n=8 each) using a random number table: sham operation group (Sham group), group I/R, sevoflurane postconditioning group (group SP), and microtubule depolymerizer colchicine plus sevoflurane postconditioning group (group CSP). Myocardial I/R was produced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion in I/R, SP and CSP groups.Colchicine 0.04 μmol/kg was intraperitoneally injected at 30 min before ischemia in group CSP.In SP and CSP groups, 2.4% sevoflurane was inhaled for 15 min starting from onset of reperfusion.Mice were sacrificed at 120 min of reperfusion, and myocardial specimens were obtained for determination of myocardial infarct size and expression of α-tubulin (by Western blot). Results Compared with group Sham, the myocardial infarct size was significantly increased, and the expression of α-tubulin was down-regulated in the other three groups (P 0.05). Compared with group SP, the myocardial infarct size was significantly increased, and the expression of α-tubulin was down-regulated in group CSP (P<0.05). Conclusion The mechanism by which sevoflurane postconditionning reduces myocardial I/R injury is related to stabilizing microtubule structure of mice. Key words: Anesthetics, inhalation; Ischemic postconditionning; Myocardial reperfusion injury; Microtubules
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Objective To evaluate the effect of sevoflurane postconditioning on microtubule structure during myocardial ischemia-reperfusion (I/R) in mice. Methods Thirty-two healthy male C57 mice, aged 7-8 weeks, wighing 20-30 g, were divided into 4 groups (n=8 each) using a random number table: sham operation group (Sham group), group I/R, sevoflurane postconditioning group (group SP), and microtubule depolymerizer colchicine plus sevoflurane postconditioning group (group CSP). Myocardial I/R was produced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion in I/R, SP and CSP groups.Colchicine 0.04 μmol/kg was intraperitoneally injected at 30 min before ischemia in group CSP.In SP and CSP groups, 2.4% sevoflurane was inhaled for 15 min starting from onset of reperfusion.Mice were sacrificed at 120 min of reperfusion, and myocardial specimens were obtained for determination of myocardial infarct size and expression of α-tubulin (by Western blot). Results Compared with group Sham, the myocardial infarct size was significantly increased, and the expression of α-tubulin was down-regulated in the other three groups (P 0.05). Compared with group SP, the myocardial infarct size was significantly increased, and the expression of α-tubulin was down-regulated in group CSP (P<0.05). Conclusion The mechanism by which sevoflurane postconditionning reduces myocardial I/R injury is related to stabilizing microtubule structure of mice. Key words: Anesthetics, inhalation; Ischemic postconditionning; Myocardial reperfusion injury; Microtubules
Key concepts: Sevoflurane, Myocardial infarction, Reperfusion injury, Colchicine, Medicine, Ischemia, Anesthesia, Microtubule