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机构地区:[1]吉林大学基础医学院药理学教研室,吉林长春130021 [2]辽宁省沈阳市242医院预防科
出 处:《吉林大学学报(医学版)》2009年第5期794-797,F0002,共5页Journal of Jilin University:Medicine Edition
基 金:国家自然科学基金资助课题(30472020)
摘 要:目的:探讨蒺藜皂苷(GSTT)对大鼠心肌缺血再灌注损伤的保护作用,阐明其基本作用机制。方法:36只雄性Wistar大鼠随机分为假手术组、再灌注模型组、阳性药血塞通(20.0 mg.kg-1)组及GSTT高、中、低(30.0、15.0和7.5 mg.kg-1)剂量组,每组6只,结扎冠状动脉前降支30 min,松扎再灌注120 min制备心肌缺血再灌注损伤模型,检测血清中SOD、MDA、CK、AST、LDH及NO含量,观察其对心肌组织病理形态学的影响。结果:与假手术组比较,模型组心肌细胞水肿明显,胞质着色较浅,胞核浓缩及深染。GSTT高、中剂量组和阳性药组上述改变较模型组明显减轻,维持细胞的正常形态。与假手术组比较,模型组大鼠血清AST、LDH、CK和MDA含量升高(P<0.01),SOD和NO含量降低(P<0.01)。与模型组比较,GSTT高、中剂量组和阳性药组可使AST、LDH、CK和MDA含量明显降低(P<0.05或P<0.01),SOD和NO含量增加(P<0.05或P<0.01)。结论:GSTT对大鼠缺血再灌注心肌组织具有保护作用,其可能与抗脂质过氧化反应有关。Objective To investigate the protective effect of Gross Saponin Tribulus Terrestris(GSTT) on the rat myocardial ischemia-reperfusion models and its mechanism.Methods Thirty-six male Wistar rats were divided randomly into sham group,ischemia-reperfusion model group,Xue-Sai-Tong(20 mg·kg^-1) group and GSTT(30.0,15.0,7.50 mg·kg^-1) groups(n=6).The myocardial ischemia-reperfusion model was induced by 30 min left anterior descending coronary occulusion and 120 min reperfusion in openchest anesthetized rats.The cardiocyte morphological changes were observed and the contents of SOD,MDA,CK,AST,LDH and NO in serum were detected.Results Compared with sham group,the cardiocytes had serious edema and cytoplasm was stained slightly and nucleus were contracted and strained deeply after reperfusion in model group.In GSTT(30 and 15 mg·kg-1) groups and Xue-Sai-Tong group the cellular edema was reduced,the cadiocytes maintained normal appearance.Compared with sham group,the contents of AST,LDH,CK and MDA in model group were increased but SOD and NO were decreased(P〈0.01).Compared with model group,in GSTT(30 and 15 mg·kg-1) groups and Xue-Sai-Tong group the contents of MDA,AST,LDH and CK were decreased,and the contents of SOD and NO were increased(P〈0.05 or P〈0.01).Conclusion GSTT has the protective effects on myocardial ischemia-reperfusion injury in rats,which may be related to inhibition of lipid oxidation and modulation of endogenous antioxidant enzyme activities.
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