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目的:研究知母皂苷OfficinalisininⅠ对心肌缺血损伤的保护作用,并进一步探讨其可能的作用机制。方法:大鼠随机分为空白对照、模型对照、知母皂苷600mg/kg、知母皂苷300mg/kg、知母皂苷150mg/kg与地奥心血康120mg/kg(阳性对照)共6组,异丙肾上腺素制备大鼠急性心肌缺血模型。除空白对照外,每日灌胃给药,治疗5天。观察各组心肌组织的病理学变化以及检测各组的血清中磷酸肌酸激酶(CK)、乳酸脱氢酶(LDH)、天冬氨酸氨基转移酶(AST)含量变化。检测心肌组织中谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、活性氧(ROS)、超氧化物歧化酶(SOD)、血红素加氧酶-1(HO-1)、p53、Bcl-2和Bax的活性。结果:病理检查可以看出,相比模型对照,知母皂苷600mg/kg组肌束排列较为整齐,肌纤维没有明显的肿胀、断裂;知母皂苷600mg/kg组CK、AST、LDH、MDA、Bax、p53、ROS含量或活性显著降低;GSH-Px、SOD、Bcl-2活性显著增加。结论:知母皂苷具有保护心肌缺血损伤的作用,其可能的作用机制与抗自由基、抑制细胞凋亡有关。
OBJECTIVE: To study the protective effects of Officinalisinin I on myocardial ischemic injury and to explore its possible mechanism. Methods: The rats were randomly divided into 6 groups: blank control, model control, timosaponin 600mg / kg, timosaponin 300mg / kg, timosaponin 150mg / kg and Diaoqixuekang 120mg / kg (positive control) Preparation of acute myocardial ischemia model in rats. In addition to the blank control, daily gavage, for 5 days. The pathological changes of myocardium in each group were observed, and the contents of CK, LDH and AST in serum of each group were detected. The levels of glutathione peroxidase (GSH-Px), malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD), heme oxygenase-1 ), P53, Bcl-2 and Bax activity. Results: Compared with the model control, the muscle bundles of 600mg / kg timosaponin were arranged neatly, and there was no obvious swelling and rupture of the muscle fibers. CK, AST, LDH, MDA, Bax , P53, ROS content or activity decreased significantly; GSH-Px, SOD, Bcl-2 activity increased significantly. Conclusion: Timosaponin has protective effect on myocardial ischemia and its possible mechanism is related to anti-free radical and inhibition of apoptosis.