摘要
背景动脉粥样硬化(AS)会引发心肌梗死、心肌纤维化等心血管病变,随着全球人口老龄化加重,发病人群逐渐增多。炎症反应是心肌纤维化的关键因素,规律的有氧运动可以减轻炎症保护心肌功能。但有氧运动对AS心肌纤维化的保护机制尚不清楚。目的本研究旨在探讨有氧运动对AS小鼠心肌纤维化的影响机制。方法2022年2—8月选取27只8周龄的雄性ApoE^(-/-)小鼠作为实验对象,将小鼠随机分为对照组、模型组和有氧运动组,每组9只。制备AS小鼠模型,对小鼠进行运动训练,Masson染色、苏木素-伊红(HE)染色观察心肌组织情况,蛋白质印迹法(Western blotting)检测心肌组织NOD受体3(NLRP3)、白介素1β(IL-1β)、转化生长因子β1(TGF-β1)蛋白表达情况,检测超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)表达量。结果Masson染色结果示模型组心肌组织纤维化较对照组明显加重;有氧运动组心肌组织纤维化较模型组明显改善。HE染色结果示模型组小鼠心肌细胞排列较错乱,细胞形态、大小异常,细胞间隙增大,存在炎性细胞浸润;有氧运动组小鼠心肌细胞排列尚整齐,细胞形态、大小异常,细胞间隙基本正常。模型组NLRP3、IL-1β、TGF-β1蛋白表达高于对照组,有氧运动组NLRP3、IL-1β、TGF-β1蛋白表达低于模型组、高于对照组(P<0.05)。模型组SOD、GSH-Px表达量低于对照组,有氧运动组SOD、GSH-Px表达量高于模型组、低于对照组(P<0.05)。结论有氧运动明显改善ApoE^(-/-)AS小鼠心肌纤维化,其机制可能与抑制心肌炎性反应、激活抗氧化水平有关。
Background Atherosclerosis(AS)causes cardiovascular diseases such as myocardial infarction and myocardial fibrosis.Incidence of the population gradually increases with the aging of the global population.The inflammatory response is a key factor in myocardial fibrosis,and regular aerobic exercise can reduce inflammation and protect myocardial function.However,the protective mechanism of aerobic exercise against AS myocardial fibrosis is unclear.Objective To investigate the mechanism of the effect of aerobic exercise on myocardial fibrosis in AS mice.Methods From February to August 2022,twenty-seven 8-week-old male ApoE^(-/-)mice were selected as the experimental subjects and randomly divided into the control group,model group and aerobic exercise group,with 9 mice in each group.The mouse model of AS was prepared,and the mice were trained with exercise.The myocardial tissue was observed by hematoxylin-eosin(HE)and Masson staining.The protein expressions of NOD receptor 3(NLRP3),interleukin1β(IL-1β)and transforming growth factorβ1(TGF-β1)in myocardial tissue were detected by Western blotting.The expressions of superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)were detected.Results Masson staining results showed that myocardial fibrosis in the model group was significantly worse than that in the control group.Myocardial fibrosis in the aerobic exercise group was significantly improved compared with the model group.HE staining showed that myocardial cells in the model group were disorganized,with abnormal cell morphology and size,enlarged cell gaps and inflammatory cell infiltration.Cardiomyocytes of mice in the aerobic exercise group were still neatly arranged,with abnormal cell morphology and size,and the cell gap was basically normal.The expressions of NLRP3,IL-1βand TGF-β1 in the model group were higher than those in the control group,while the expressions of NLRP3,IL-1βand TGF-β1 in the aerobic exercise group were lower than those in the model group,and higher than the control group(P<0.05).The expressions of SOD and GSH-Px in the model group were lower than those in the control group,and the expressions of SOD and GSH-Px in the aerobic exercise group were higher than those in the model group,and lower than those in the control group(P<0.05).Conclusion Aerobic exercise significantly improved myocardial fibrosis in ApoE^(-/-)AS mice,and the mechanism may be related to inhibiting myocardial inflammatory response and activating antioxidant levels.
作者
秦芳
马甜甜
于子夫
刘西花
QIN Fang;MA Tiantian;YU Zifu;LIU Xihua(College of Rehabilitation,Shandong University of Traditional Chinese Medicine,Jinan 250355,China;Rehabilitation Department,Affiliated Hospital of Shandong University of Traditional Chinese Medicine,Jinan 250014,China)
出处
《中国全科医学》
北大核心
2024年第5期557-562,共6页
Chinese General Practice
基金
国家自然科学基金青年基金项目(81802239)。
