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目的:探讨右丙亚胺对蒽环类药物(阿霉素)引起的心脏毒性模型大鼠的心脏保护效应以及其相关作用机制。方法:选择50只成年雌性Wistar大鼠,随机分为正常对照组、模型组、右丙亚胺低剂量组12.5mg/kg、右丙亚胺中剂量组25mg/kg、右丙亚胺高剂量组37.5mg/kg,每组10只。每周给药一次,观察一般生命体征,给药6周后,处死大鼠,采集血清检测超氧化物歧化酶(SOD)、丙二醛(MDA)、肌钙蛋白I(cTnI),并进行心脏病理学检查。结果:模型组大鼠MDA与cTnI表达量高于正常对照组和右丙亚胺各剂量组,而SOD表达量则低于正常对照组和右丙亚胺各剂量组。与模型组比较,右丙亚胺各剂量组MDA与cTnI表达量均有不同程度降低,其中右丙亚胺中、高剂量均有统计学意义(P<0.05);右丙亚胺各剂量组SOD表达量则均不同程度升高,其中右丙亚胺中、高剂量均有统计学意义(P<0.05);右丙亚胺可在一定程度上减轻心肌病理损伤。结论:大鼠注射阿霉素后,可致心脏毒性,引起MDA与cTnI表达升高,SOD水平降低;右丙亚胺可升高SOD水平,降低MDA与cTnI表达量,对心脏毒性有一定的保护作用,其作用机制可能与降低脂质过氧化与减轻对于心肌细胞损伤有关。
AIM: To investigate the cardioprotective effect of dexmedetomidine on cardiotoxicity induced by anthracycline (doxorubicin) in rats and its related mechanisms. Methods: Fifty adult female Wistar rats were randomly divided into normal control group, model group, dexrazoxane low dose group 12.5mg / kg, dexrazoxane middle dose group 25mg / kg, dexrazoxane high dose Group 37.5mg / kg, each group of 10. The rats were administered once a week for observation of general vital signs. After 6 weeks of administration, the rats were killed and the serum samples were taken for detection of superoxide dismutase (SOD), malondialdehyde (MDA) and troponin I (cTnI) Cardiopathological examination. Results: The expression of MDA and cTnI in model group was higher than that in normal control group and dexrazoxane, while the expression of SOD in model group was lower than that in normal control group and dexrazoxane group. Compared with the model group, the expression levels of MDA and cTnI in all doses of dexrazoxane decreased to different extents, and the middle and high doses of dexrazoxane were statistically significant (P <0.05) SOD levels were increased to varying degrees, of which dexrazoxane middle and high doses were statistically significant (P <0.05); dexpropimide can reduce myocardial damage to some extent. Conclusion: Rats injected with doxorubicin can induce cardiotoxicity and induce the expression of MDA and cTnI to increase and the level of SOD decrease. Depridin can increase the level of SOD and decrease the expression of MDA and cTnI, and have certain cardiotoxicity The protective effect may be related to the reduction of lipid peroxidation and mitigation of cardiomyocyte injury.