摘要
目的:探讨烟酰胺(Nic)对阿霉索(ADR)所致实验性心肌损伤的保护作用及其机制。方法:选取Wistar大鼠,随机分为正常对照组、阿霉素(ADR)组和Nic Ⅰ、Nic Ⅱ、Nic Ⅲ3个实验组,采用多次腹腔注射ADR,复制慢性心肌损伤模型,5周后进行离体心脏血液动力学及左心室功能指标、心肌SOD、GSH—PX及MDA含量测定,并进行心肌的电镜形态学观察。结果:多次注射ADR所致慢性心肌损伤模型中大鼠心脏功能明显降低,心肌SOD及GSH-PX活性显著下降,MDA含量明显升高,同时出现心肌细胞超微结构的损伤。Nic(100mg/kg、200mg/kg、4 00 mg/kg)能明显改善血液动力学及心功能各项指标,显著增加SOD、GSH—PX活性,降低MDA含量,减轻心肌细胞超微结构的损伤。结论:Nic对阿霉素所致的慢性心肌损伤有保护作用,其机制可能与抗自由基从而防止脂质过氧化并在此基础上改善心脏舒缩功能有关。
Objective: AIM : To investigate the protective effects of nicotinamide (Nic) on experimental myocardial injury induced by adriamycin (ADR) in rats and its mechanisms. Methods: Wistar rats (n = 60) were randomly divided into Normal, ADR, Nic Ⅰ , Nic Ⅱ and Nic Ⅲ groups. The myocardial injury model was established by peritoneum injection of ADR several times. 5-week the left ventricular function, the levels of SOD, GSH-PX and MDA in myocardium which were perfused in a Langcndorff mode was measured later, and the changes of the ultrastructure of myocardium were observed by electron microscope. Results: In rats only received ADR, the left ventricular function and the activities of SOD and GSH-PX in myocardium were decreased, and the content of MDA was increasd, as well as the destruction of ultrastructure of myocardium emerged. Nic (100 mg, 200 mg, 300 mg/kg) could improve the left ventricular function which decreased by ADR, increase the activities of SOD and GSH-PX, decrease the content of MDA and prevent the destruction on ultrastructure of myocardium from ADR. Conclusion: Nic has the protective characters on experimental myocardial injury induced by ADR. The mechanism is probably related to inhibiting lipid pcroxidation and improving systole and diastole of heart.
出处
《新疆医科大学学报》
CAS
2003年第6期569-572,共4页
Journal of Xinjiang Medical University
关键词
烟酰胺
阿霉素
心肌损伤
血液动力学
脂质过氧化
nicotinamide
adriamycin
myocardial injury
hemodynamics
lipid peroxidation
