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机构地区:[1]钦州市第二人民医院药剂科,广西钦州535099
出 处:《中国实验方剂学杂志》2013年第10期265-268,共4页Chinese Journal of Experimental Traditional Medical Formulae
摘 要:目的:研究三七皂苷R1对垂体后叶素诱导急性心肌缺血(AMI)大鼠的影响。方法:SD大鼠随机分成5组:正常组、模型组、地尔硫艹卓阳性药组(5 mg.kg-1)和三七皂苷R1组(5,10 mg.kg-1)。连续给药7 d,末次给药1 h后,观察给药后AMI大鼠心电图的变化。取血,检测血浆门冬氨酸转氨酶(AST)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、乳酸脱氢酶同工酶-1(LDH1)水平。双重染色法测定心肌缺血面积。HE染色观察心肌组织病理学变化。Westernblot法检测心脏组织B细胞淋巴瘤-白血病-2(Bcl-2),B-细胞白血病淋巴瘤-2-相关X蛋白(Bax)蛋白的表达。结果:与模型组比较,三七皂苷R1可降低ST段抬高值,有效减少血浆心肌酶的水平(P<0.05),明显减少AMI大鼠心肌缺血面积(P<0.01),并改善心肌缺血病理性损伤。同时上调心脏组织中Bcl-2蛋白表达,同时下调Bax蛋白的水平(P<0.01)。结论:三七皂苷R1对AMI大鼠具有保护作用,其机制可能与减少心肌酶释放以及抑制心肌细胞凋亡有关。Objective: To study the protective effect of notoginsenoside R1 on acute myocardial ischemia (AMI) in rats. Method: The SD rats were randomly assigned to 5 groups: normal group, model group, diltiazem group (5 mgkg-1), notoginsenoside R1 groups (5, 10 mgkg-1, respectively). The changes of electrocardiogram in AMI rats were observed after treatment. The levels of aspartete transaminase (AST), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), and lactate dehydrogenase-1 (LDH1) in serum were detected and analyzed. The double staining method was used for the determination of the ischemic area. Additionally, the histopathological changes of cardiac tissue were observed of by HE staining.The expression of B cell lymphoma/leukemia-2(Bcl-2), Bcl-2-associated X protein(Bax) proteins in cardiac tissue were observed using Western blot analysis. Result: Compared to model group, notoginsenoside R1 lessened the elevation value of ST-segment and inversion rate of T-wave (P〈0.01), and effectively reduced the levels of myocardium enzyme in serum (P〈0.05), in addition, notably reduced the area of myocardial ischemia in AMI rats (P〈0.01). And the pathological damages of myocardial ischemia were improved. Meanwhile, the expression of Bcl-2 protein in heart tissue was increased, whereas the level of Bax protein was decreased (P〈0.01). Conclusion: The results suggest that notoginsenoside R1 has protective effect on AMI rats, and mechanisms may be related to lessening the release of myocardium enzyme in serum and inhibiting the apoptosis of cardiomyocyte.
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