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目的观察11,12-环氧二十碳三烯酸(11,12-EET)预处理与后处理对缺血/再灌注(IR)大鼠心肌钙调节蛋白的影响,探讨11,12-EET心肌保护的作用及其机制。方法采用Langendorff离体灌流装置,通过停灌40min/复灌30min复制大鼠心肌IR损伤模型。将33只雄性Sprague-Dawley大鼠随机分为对照组、IR组、EET预处理组(Pre-EET)及EET后处理组(Post-EET)。采用BL-420生物信号采集系统监测心功能,比色法检测肌浆网Ca2+-ATPase变化,半定量RT-PCR方法检测钙泵(SERCA)、磷酸受纳蛋白(PLB)、兰尼碱受体2型(RyR2)及1,4,5-三磷酸肌醇受体2型(IP3R2)表达变化。结果Pre-EET及Post-EET组与IR组相比,心功能改善、Ca2+-ATPase活性增高(P<0.05,P<0.01);IP3R2表达增强,PLB表达降低(P<0.05,P<0.01);Pre-EET组SERCA表达增强(P<0.05)。Pre-EET与Post-EET组间差异无显著性;各组RyR2表达差异无显著性。结论11,12-EET预处理与后处理具有拮抗IR损伤的作用,这与其诱导肌浆网IP3R2表达上调,PLB表达下调以及改善Ca2+-ATPase的活性有关;同时,预处理肌浆网SERCA表达上调,也可能是其抗IR损伤机制之一。
Objective To investigate the effects of 11,12-epothilonic acid (11,12-EET) preconditioning and postconditioning on myocardial calcineurin in rats with ischemia / reperfusion (IR) The role of myocardial protection and its mechanism. Methods Langendorff isolated perfusion device was used to replicate myocardial IR injury model by stopping ischemia for 40min and reperfusion for 30min. Thirty-three male Sprague-Dawley rats were randomly divided into control group, IR group, EET pretreatment group and Post-EET group. Cardiac function was monitored by BL-420 biosignal acquisition system. Ca2 + -ATPase was detected by colorimetric assay. Serum calcium, SERCA, PLB, 2 (RyR2) and inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) expression changes. Results Compared with the IR group, the cardiac function and the activity of Ca2 + -ATPase in the Pre-EET and Post-EET groups were significantly increased (P <0.05, P <0.01); the expression of IP3R2 was enhanced and the PLB expression was decreased ; Pre-EET group, SERCA expression was enhanced (P <0.05). There was no significant difference between Pre-EET and Post-EET groups. There was no significant difference in RyR2 expression between groups. Conclusion Pretreatment and postconditioning of 11,12-EET can antagonize IR injury, which is related to up-regulation of IP3R2 expression, down-regulation of PLB expression and improvement of Ca2 + -ATPase activity in sarcoplasmic reticulum, and up-regulation of SERCA expression in sarcoplasmic reticulum , It may also be one of its anti-IR damage mechanism.