【摘要】 目的研究没食子酸在心肌梗死后心肌纤维化中的作用及机制。方法结扎小鼠冠状动脉前降支制备心肌梗死模型,将30只造模成功的小鼠随机分为假手术组、心肌梗死模型组、没食子酸干预组,每组10只。没食子酸干预组给予没食子酸(100mg/kg/d)腹腔注射,其他组腹腔注射等量的生理盐水,连续14天。14天后观察各组间心功能和心肌纤维化差别。结果①与心肌梗死模型组比较,没食子酸干预组小鼠左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)显著降低,左室缩短率(LVFS)显著升高(P<0.001);②与心肌梗死模型组比较,没食子酸干预组心脏心钠肽(ANP)、B型脑钠肽(BNP)、Ⅰ型胶原(CollagenⅠ)、纤维粘连蛋白(Fibronectin)、组蛋白去乙酰化酶5(HDAC5)、基质金属蛋白酶9(MMP9)表达水平降低(P<0.001)。结论没食子酸可抑制心肌梗死后心肌纤维化,改善心功能,其机制可能与HDAC5信号通路有关。更多还原

【Abstract】 Objective To investigate the role and mechanism of gallic acid on myocardial fibrosis after myocardial infarction.Methods The myocardial infarction models were established by ligating the left anterior descending coronary artery of mice.Thirty male models were divided into sham group(10),myocardial infarction model group(10)and gallic acid group(10).Mice of gallic acid group were continuously treated with gallic acid(100 mg/kg/day)for 14 days by intraperitoneal injection.Mice of other groups were injected with an equal amount of normal saline.After 14 days,the cardiac function and myocardial fibrosis were measured and the difference were compared among three groups.Results ①Compared with myocardial infarction model group,LVEDD and LVESD were decreased,while LVFS was increased in the gallic acid injected group(P<0.01).②Compared with myocardial infarction model group,the expression levels of ANP,BNP,collagenⅠ,fibronectin,HDAC5 and MMP9 were significantly decreased in the gallic acid group(P<0.01).Conclusion Gallic acid can significantly inhibit myocardial fibrosis after myocardial infarction,improve ventricular function,mainly through inhibition of HDAC5 signal pathway.更多还原