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Anti-inflammatory and Anti-endoplasmic reticulum stress Effects of catalpol Against myocardial ischemia-reperfusion injury in streptozotocin-induced diabetic rats

机译:抗炎症和抗内质网胁迫对链脲佐菌素诱导糖尿病大鼠心肌缺血再灌注损伤的抗炎和抗内质网胁迫影响

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The current study was designed to investigate the effects and the mechanism of catalpol on myocardial ischemia-reperfusion (MI/R) injury in a diabetic rat model. Male Sprague-Dawley rats were divided into DM + sham, DM +I/R, and DM +I/R + C groups and diabetes was induced using single injections of streptozotocin (STZ; 70 mg/kg; i.p). After confirming the induction of diabetes, rats were administered physiological saline and catalpol (10 mg/kg; i.p.) daily for 28 days. Subsequently, rats were subjected to left anterior descending (LAD) coronary artery occlusion for 30 min followed by reperfusion for 2 h. Haemodynamic parameters were recorded throughout surgery, and following sacrifice, hearts were isolated for biochemical, histopathological, and molecular analyses. Catalpol treatment significantly ameliorated MI/R injury by improving cardiac function, normalizing myocardial enzyme activities and markers of oxidative stress, and by maintaining myocardial architecture. Furthermore, expression levels of the in?ammatory cytokines TNF-α and IL-6 were decreased in biochemical and immunohistochemical studies. Additionally, the cardioprotective effects of catalpol were partly related to reductions in myocardial endoplasmic reticulum stress (ERS). In conclusion, catalpol exerts cardioprotective effects in diabetic rats by attenuating in?ammation and inhibiting ERS.
机译:目前的研究旨在探讨试潮对糖尿病大鼠模型中心肌缺血再灌注(MI / R)损伤的影响和机制。使用单一注射链脲佐菌素(STZ; 70 mg / kg; i.p),将雄性Sprague-Dawley大鼠分为DM + Sham,DM + I / R和DM + I / R + C组和糖尿病。在确认糖尿病诱导后,每天28天每天施用生理盐水和催化剂(10mg / kg; i.p.)。随后,对大鼠进行左前期下降(LAD)冠状动脉闭塞30分钟,然后再灌注2小时。血液动力学参数在整个手术中记录,并在牺牲后,孤立的生物化学,组织病理学和分子分析。通过改善心脏功能,使心肌酶活性和氧化应激标记标记,并通过维持心肌架构,对Catalpol治疗显着改善Mi / R损伤。此外,生物化学和免疫组织化学研究中,INα甜型细胞因子TNF-α和IL-6的表达水平降低。另外,Catalpol的心脏保护作用部分与心肌内质网胁迫(ERS)的减少有关。总之,通过衰减α混合物和抑制剂,Catalpol在糖尿病大鼠中施加心脏保护作用。

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