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作 者:张诗琴 刘子奇 李彬[1] 贺轶宇[1] 蒋学俊[1] ZHANG Shiqin;LIU Ziqi;LI Bin;HE Yiyu;JIANG Xuejun(Department of Cardiology,Renmin Hospital of Wuhan University,Cardiovascular Research Institute,Wuhan University,Hubei Key Laboratory of Cardiology,Wuhan 430060,Hubei,China)
机构地区:[1]武汉大学人民医院心内科、武汉大学心血管病研究所、心血管病湖北省重点实验室,武汉湖北430060
出 处:《心血管病学进展》2024年第8期757-761,768,共6页Advances in Cardiovascular Diseases
基 金:国家自然科学基金(81800444);湖北省自然科学基金(2018CFB415)。
摘 要:目的探讨运动对心肌梗死(MI)诱发大鼠心室重塑的影响及相关机制。方法对成年雄性Sprague-Dawley大鼠进行冠状动脉左前降支结扎,建立MI模型。大鼠被分为三组:对照组(sham组)、MI-久坐组(MI-Sed组)和MI-运动组(MI-Ex组)。MI-Ex组大鼠在MI建模手术后1周开始运动训练,为期4周,每周运动6 d。运动干预结束后,对各组大鼠进行研究。超声心动图用于评估心脏结构和功能。组织学分析用于评估心肌纤维化和肥厚等病理变化。用Western blotting评估核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3(NLRP3)相关炎症因子水平。结果MI大鼠表现出心脏结构和功能异常、心脏肥大和心肌间质纤维化,并伴有较高的NLRP3炎症小体表达。运动4周后,随着NLRP3炎症小体被抑制,MI大鼠的心脏功能得到改善,心肌肥厚和心肌间质纤维化减轻。结论NLRP3炎症小体在MI诱导的心室重塑模型中被激活。运动可改善心脏功能,其机制与NLRP3炎症小体活化的减弱有关。Objective To explore effects of exercise on myocardial infarction(MI)-induced ventricular remodeling and the related mechanisms in rats.Methods Adult male Sprague-Dawley rats underwent the left anterior descending coronary artery ligation to generate MI model.The rats were divided into three groups:sham group,MI-sedentariness(MI-Sed)group,MI-exercise(MI-Ex)group.Rats in the MI-Ex group started exercise training 1 week after the MI surgery and lasted for a period of 4 weeks,with 6 days of exercise per week.Rats in all groups were studied at the end of the exercise intervention.Echocardiography was used to evaluate cardiac structure and function.Histological analysis was used to assess pathological changes such as myocardial fibrosis and hypertrophy.Western blotting was used to evaluate nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3)inflammasome.Results MI rats exhibited abnormal cardiac structure and function,cardiac hypertrophy,and myocardial interstitial fibrosis,accompanied by higher NLRP3 inflammasome expression.4 weeks after exercise,cardiac function was improved in MI rats,cardiac hypertrophy and myocardial interstitial fibrosis was attenuated,with NLRP3 inflammasome inhibition.Conclusion NLRP3 inflammasome was activated in MI-induced ventricular remodeling model.Exercise improved cardiac function,the mechanisms accompanied by attenuation NLRP3 inflammasome activation.
分 类 号:R542.22[医药卫生—心血管疾病]
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