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作 者:朴哲浩 王天娇 金丽 崔燕[3] PIAO Zhe-hao;WANG Tianjiao;JIN Li(Department of Cardiology,The Second Affiliated Hospital of Wenzhou Medical University,Wenzhou 325027,China)
机构地区:[1]温州医科大学附属第二医院心血管内科,浙江温州325000 [2]中国医学科学院阜外医院深圳医院心血管内科 [3]吉林大学第二医院心血管内科
出 处:《中国实验诊断学》2020年第5期846-850,共5页Chinese Journal of Laboratory Diagnosis
基 金:温州市科技局基础性医疗卫生科技项目(Y20190413)。
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。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(100mg/kg/day)for 14days by intraperitoneal injection.Mice of other groups were injected with an equal amount of normal saline.After 14days,the cardiac function and myocardial fibrosis were measured and the difference were compared among three groups.Results①Compared 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,HDAC5and MMP9were 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 HDAC5signal pathway.
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