Role of SphK1/S1P signaling pathway in adiponectin-induced restoration of attenuation of myocardial ischemia-reperfusion injury by sevoflurane postconditioning in diabetic rats
10.3760/cma.j.cn131073.20191110.00626
- VernacularTitle:SphK1/S1P信号通路在脂联素恢复七氟烷后处理减轻糖尿病大鼠心肌缺血再灌注损伤中的作用
- Author:
Xianliang XING
1
;
Na ZHENG
;
Jing ZHANG
;
Yanhui HU
;
Qin LIU
Author Information
1. 南昌大学第二附属医院麻醉科 330006
- From:
Chinese Journal of Anesthesiology
2020;40(6):747-751
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the role of SphK1/S1P signaling pathway in adiponectin-induced restoration of attenuation of myocardial ischemia-reperfusion (I/R) injury by sevoflurane postconditioning in diabetic rats.Methods:Healthy clean-grade male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, in which diabetes mellitus was induced by combination of high-fat and high-sucrose diet and intraperitoneal injection of 1% streptozotoein in citric acid buffer 40 mg/kg, were studied.Ninety rats with diabetes mellitus were divided into 6 groups ( n=15 each) using a random number table method: sham operation group (group Sham), group I/R, sevoflurane postconditioning group (group S), adiponectin preconditioning group (group A), adiponectin preconditioning+ sevoflurane postconditioning group (group AS) and adiponectin preconditioning+ K6PC-5 (a specific SphK1 activator)+ sevoflurane postconditioning group (group AKS). Myocardial I/R was induced by 30 min occlusion of anterior descending branch of left coronary artery followed by 120 min reperfusion.At 15 min before ischemia, recombinant adiponectin 5.0 μg/g was injected intraperitoneally in A, AS and AKS groups, and K6PC-5 1 μg/g was injected via the tail vein in group AKS.In S, AS and AKS groups, 2.5% sevoflurane was inhaled for 5 min starting from the onset of reperfusion.Blood samples from the internal jugular vein were collected at the end of reperfusion for determination of serum cardiac troponin I (cTnI) concentration (by enzyme-linked immunosorbent assay), percentage of myocardial infarct volume (by TTC staining) and expression of SphK1, S1P and phosphorylated NF-κB p65 (p-NF-κB p65) in myocardial tissues (by Western blot). Results:Compared with group Sham, the serum cTnI concentration and percentage of myocardial infarct volume were significantly increased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was up-regulated in group I/R ( P<0.05). Compared with group I/R, no significant change was found in each parameter in group S ( P>0.05), and the serum cTnI concentration and percentage of myocardial infarct volume were significantly decreased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was down-regulated in group A ( P<0.05). Compared with group S, the serum cTnI concentration and percentage of myocardial infarct volume were significantly decreased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was down-regulated in group AS ( P<0.05). Compared with group AS, the serum cTnI concentration and percentage of myocardial infarct volume were significantly increased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was up-regulated in group AKS ( P<0.05). Conclusion:SphK1/S1P signaling pathway is involved in adiponectin-induced restoration of attenuation of myocardial I/R injury by sevoflurane postconditioning in diabetic rats.
