辣椒素降低线粒体氧化应激水平拮抗心脏缺血再灌注损伤的研究

发布时间：2018-04-27 21:39

本文选题：辣椒素 + 线粒体氧化应激　；参考：《四川大学学报(医学版)》2017年05期

【摘要】：目的探讨辣椒素(CAP)对心脏缺血再灌注损伤的保护作用及可能机制。方法 24只SD雄性大鼠随机分为4组(n=6):(1)对照组,(2)缺血再灌注组(IR组),(3)CAP干预缺血再灌注组(CAP+IR组),(4)辣椒素受体拮抗剂辣椒平(CAPZ)预处理后加CAP干预缺血再灌注组(CAPZ+CAP+IR组)。采用大鼠离体心脏Langendorff灌流方法,再灌注30min末以左室发展压(LVDP)和左室舒张末压(LVEDP)评价心脏功能。测定再灌注开始后前5min冠脉流出液中乳酸脱氢酶(LDH)的含量。再灌注120min后取心脏,采用2、3、5-氯化三苯基四氮唑(TTC)染色法评价心肌梗死面积的变化;HE染色观察心肌纤维形态学变化;线粒体氧化应激检测试剂盒检测超氧化物歧化酶(SOD)和丙二醛(MDA)。再灌注10min取心脏组织,Western blot检测细胞色素c和caspase-3蛋白表达。结果与对照组相比,IR组LVEDP升高、LVDP降低(P0.01),心肌梗死面积增大(P0.01),心肌纤维排列紊乱,线粒体SOD活性降低、MDA质量摩尔浓度增加(P0.01),冠脉流出液中LDH含量增多(P0.01),caspase-3、细胞色素c蛋白的表达量增加(P0.01);与IR组比较,CAP+IR组LVEDP降低、LVDP部分恢复(P0.01),心肌梗死面积减小(P0.01),心肌纤维断裂减少,线粒体SOD活性增加,MDA质量摩尔浓度减少(P0.01),冠脉流出液中LDH含量减少(P0.01),caspase-3和细胞色素c蛋白表达量降低(P0.01);但CAPZ可阻断CAP的上述保护作用。结论 CAP可通过降低线粒体氧化应激减少缺血再灌注引起的细胞坏死和凋亡,改善心脏功能,减轻大鼠离体心脏缺血再灌注损伤。
[Abstract]:Objective to investigate the protective effect of capsaicin (capsaicin) on myocardial ischemia reperfusion injury and its possible mechanism. Methods Twenty-four male Sprague-Dawley rats were randomly divided into 4 groups: control group (n = 6: 1) control group (n = 2) IR group (n = 4) capsaicin receptor antagonist capsaicin (capsaicin) and capsaicin receptor antagonist (capsaicin). Capsaicin receptor antagonist capsaicin (capsaicin) was pretreated with capsaicin receptor antagonist (capsaicin) and CAP was added to the ischemia reperfusion group (CAPZ CAP IR group). Left ventricular progressive pressure (LVDP) and left ventricular end-diastolic pressure (LVEDP) were used to evaluate cardiac function at the end of reperfusion 30min in isolated rat heart. The content of lactate dehydrogenase (LDH) in 5min coronary effluents before reperfusion was measured. After reperfusion with 120min, the heart was taken out and the myocardial fiber morphology was observed by HE staining and superoxide dismutase (SOD) and malondialdehyde (MDA) MDAA were detected by mitochondrial oxidative stress test kit. The expression of cytochrome c and caspase-3 protein was detected by Western blot after reperfusion with 10min. Results compared with the control group, the LVEDP of IR group increased and decreased P0.01a, the myocardial infarction area increased P0.01a, and the arrangement of myocardial fiber was disordered. Compared with IR group, the content of LDH in coronary effluents increased, and the expression of cytochrome c protein increased. Myocardial fiber breaks down, The activity of SOD in mitochondria increased and the mol concentration of MDAA decreased, while the content of LDH in coronary effluents decreased, and the expression of caspase-3 and cytochrome c in coronary effluents decreased. However, CAPZ could block the protective effect of CAP. Conclusion CAP can reduce the necrosis and apoptosis induced by ischemia / reperfusion, improve the heart function and alleviate the ischemia reperfusion injury in isolated rat heart by reducing the oxidative stress of mitochondria.
【作者单位】：西安医学院基础医学部生理教研室;西电集团医院心内科;
【基金】：陕西省教育厅科研基金(No.15JK1639) 陕西省科技厅科研基金(No.2014JM2-8164) 西安医学院博士科研启动基金项目(No.2015DOC02)资助
【分类号】：R54

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