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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。
Objective To investigate the protective effect of basic fibroblast growth factor (bFGF) on acute myocardial injury induced by isoprenaline (Iso) in rats. Methods Wistar male rats were randomly divided into 3 groups: control group, Iso injury group and bFGF preconditioning group. The pathological changes of myocardium were observed by light microscope. The myocardial enzymes were detected by biochemical methods and the myocardial tissue was detected by thiobarbituric acid fluorescence method Lipid peroxidation MDA level, DTNB direct colorimetric assay of myocardial tissue glutathione peroxidase activity, inorganic phosphorus method for determination of myocardial mitochondrial H + -ATPase hydrolysis activity. Results In the Iso group, the myocardial necrosis was more severe, the level of lipid peroxidation MDA in myocardial enzymes and myocardium was significantly increased, and the activity of glutathione peroxidase and mitochondrial H + -ATPase activity in myocardium were decreased. The bFGF pretreatment The myocardial necrosis was significantly relieved. The level of lipid peroxidase (MDA) in myocardial enzymes and myocardium was decreased, and the activity of glutathione peroxidase (POD) and mitochondrial H + -ATPase activity in myocardium were increased (P <0.05). Conclusion bFGF can reduce myocardial injury by inhibiting lipid peroxidation, increasing antioxidant enzyme activity and improving myocardial energy metabolism.