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目的:观察依达拉奉抗异丙肾上腺素诱导的心肌纤维化作用及其作用机制。方法:选择SD雄性大鼠24只随机分为对照组、模型组和依达拉奉组。模型组和依达拉奉组背部皮下注射异丙肾上腺素20.0mg/kg,第2天背部皮下注射10.0mg/kg,第3天背部皮下注射5.0mg/kg,第4天3.0mg/kg,连续1周,共10d。自由进食,给水。依达拉奉组从第2天开始给药,每日2次,连续14d。第15天处死动物,处死前观察超氧化物歧化酶(SOD)活力、丙二醛水平,处死后观察左心室质量指数(LVMI)、胶原容积分数(CVF)、Masson染色。结果:模型组大鼠丙二醛、LVMI显著高于对照组(P<0.05),SOD明显低于对照组(P<0.05),依达拉奉组大鼠LVMI显著低于模型组(P<0.01),SOD明显高于模型组。对照组CVF为(2.52±0.19)%,模型组为(17.83±0.91)%,依达拉奉组为(14.60±1.42)%。LVMI与丙二醛呈正相关(r=0.825,P=0.000);LVMI与SOD呈负相关(r=-0.594,P=0.002)。CVF与丙二醛呈正相关(r=0.860,P=0.000);CVF与SOD呈负相关(r=-0.604,P=0.002)。结论:依达拉奉具有通过减轻氧化应激达到抗异丙肾上腺素诱导的心肌纤维化作用。
Objective: To observe the effect of edaravone on isoproterenol-induced myocardial fibrosis and its mechanism. Methods: Twenty-four SD male rats were randomly divided into control group, model group and edaravone group. The model group and edaravone group were subcutaneously injected isoproterenol 20.0mg / kg on the back, subcutaneous injection of 10.0mg / kg on the second day, subcutaneous injection 5.0mg / kg on the third day, 3.0mg / kg on the fourth day, For 1 week, a total of 10d. Free to eat, water. Edaravone group from the first two days of administration, 2 times a day for 14 days. Animals were killed on the 15th day. Superoxide dismutase (SOD) activity and malondialdehyde level were observed before sacrifice. Left ventricular mass index (LVMI), collagen volume fraction (CVF) and masson staining were observed after sacrifice. Results: The levels of malondialdehyde and LVMI in the model group were significantly higher than those in the control group (P <0.05), while those in the edaravone group were significantly lower than those in the control group (P < 0.01), SOD was significantly higher than the model group. The CVF in the control group was (2.52 ± 0.19)%, that in the model group was (17.83 ± 0.91)%, and that in the edaravone group was (14.60 ± 1.42)%. LVMI was positively correlated with malondialdehyde (r = 0.825, P = 0.000); LVMI was negatively correlated with SOD (r = -0.594, P = 0.002). CVF was positively correlated with malondialdehyde (r = 0.860, P = 0.000); CVF was negatively correlated with SOD (r = -0.604, P = 0.002). Conclusion: Edaravone can prevent isoproterenol-induced myocardial fibrosis by reducing oxidative stress.