碱性成纤维细胞生长因子对大鼠急性心肌损伤保护作用的实验观察

Experimental study of protective effects of basic fibroblast growth factor on rat myocardium injured by Iso

目的研究碱性成纤维细胞生长因子(BasicFibroblastGrowthFactor,bFGF)预处理对异丙肾上腺素(Isoprenaline,Iso)致大鼠急性心肌损伤的保护机制。方法将Wistar雄性大白鼠随机分成3组:对照组、Iso损伤组、bFGF预处理组,用光镜观察心肌组织的病理变化,生化方法检测心肌酶,硫代巴比妥酸荧光方法测定心肌组织脂质过氧化物MDA的水平,DTNB直接显色法测定心肌组织谷胱甘肽过氧化物酶活性,无机磷法测定心肌线粒体H+鄄ATP酶水解活性。结果Iso损伤组心肌坏死较重,心肌酶和心肌组织脂质过氧化物MDA的水平明显增高,心肌组织谷胱甘肽过氧化物酶活性及心肌线粒体H+鄄ATP酶水解活性减低;bFGF预处理组心肌坏死明显减轻,心肌酶及心肌组织脂质过氧化物MDA的水平下降,心肌组织谷胱甘肽过氧化物酶活性及心肌线粒体H+鄄ATP酶水解活性增加(P<0.05)。结论bFGF可通过抑制脂质过氧化,提高抗氧化酶活性和改善心肌能量代谢而减轻大鼠心肌损伤。

To study the protective effects of Basic Fibroblast Growth Factor(bFGF) on the myocardial injury induced by Iso. Methods Wistar rats were divided into three groups at random. They were the control group, the Iso group and the bFGF group respectively. The pathological changes were observed by microscope. Levels of myocardial enzymes were detected by biochemical method. Levels of myocardial tissue MDA and activity of myocadial tissue GPX and myocadial mitochondrial H+-ATPase were detected. Results In the Iso group, the myocardial necrosis was more serious, levels of myocardial enzymes and MDA were increased. Activity of myocadial tissue GPX and myocadial mitochondrial H+-ATPase were decreased; In the bFGF group,the myocardial necrosis was relieved. Levels of myocardial enzymes and MDA were decreased. Activity of myocadial tissue GPX and myocadial mitochondrial H+-ATPase were increased(P < 0.05). Conclusions The bFGF can protect rat myocardium from injury by inhibiting myocardial lipid peroxidation and amelioratin energy metabolism.