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目的探讨沙棘总黄酮(TFH)对阿霉素(ADR)诱导大鼠心肌损伤的保护作用。方法选用60只SD大鼠,分别为正常对照组,ADR模型组,生脉注射液组和TFH 3个不同给药剂量治疗组。腹腔注射ADR造成心肌损伤模型,观察沙棘总黄酮对心肌组织匀浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSH-Px)和丙二醛(MDA)水平的影响并观察组织病理学改变。结果腹腔注射ADR后可致大鼠心肌明显损害,心肌SOD及GSH-Px活性下降,MDA含量升高,同时出现心肌组织的改变。应用TFH后能增加SOD及GSH-Px活性,降低MDA含量,减轻心肌组织损伤。结论 TFH对ADR所引起的心肌结构损伤和脂质过氧化有一定的保护作用,其机制可能与保护心肌SOD、GSH-Px活性及清除自由基,防止脂质过氧化有关。
Objective To investigate the protective effect of total flavonoids of sea buckthorn (TFH) on myocardial injury induced by Adriamycin (ADR) in rats. Methods Sixty Sprague-Dawley rats were randomly divided into three groups: normal control group, ADR model group, Shengmai injection group and TFH treatment group. The model of myocardial injury induced by intraperitoneal injection of ADR was observed. The effect of total flavonoids of seabuckthorn on the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) Histopathological changes. Results After intraperitoneal injection of ADR, myocardial damage was significantly induced in rats. The activity of SOD and GSH-Px in myocardium was decreased and the content of MDA was increased. Meanwhile, the myocardial tissue was changed. Application of TFH can increase the activity of SOD and GSH-Px, reduce the content of MDA, reduce myocardial tissue injury. Conclusions TFH may play a protective role in myocardial structural damage and lipid peroxidation induced by ADR. The mechanism may be related to the protection of myocardial SOD and GSH-Px activities and the clearance of free radicals and lipid peroxidation.