文章摘要
任 何,程 锦,张明明,张东伟,张 薇,耿倩雯.鸢尾素对心肌梗死后大鼠心房颤动和心房间质纤维化的影响[J].,2022,(22):4229-4234
鸢尾素对心肌梗死后大鼠心房颤动和心房间质纤维化的影响
Effects of Irisin on Atrial Fibrillation and Interstitial Fibrosis in Rats after Myocardial Infarction
投稿时间:2022-03-23  修订日期:2022-04-18
DOI:10.13241/j.cnki.pmb.2022.22.006
中文关键词: 鸢尾素  心肌梗死  房颤  间质纤维化
英文关键词: Irisin  Myocardial infarction  Atrial fibrillation  Interstitial fibrosis
基金项目:国家自然科学基金青年基金项目(81900338)
作者单位E-mail
任 何 空军军医大学唐都医院心血管内科 陕西 西安 710038 renheH0326@126.com 
程 锦 空军军医大学唐都医院心血管内科 陕西 西安 710038  
张明明 空军军医大学唐都医院心血管内科 陕西 西安 710038  
张东伟 空军军医大学唐都医院心血管内科 陕西 西安 710038  
张 薇 空军军医大学唐都医院心血管内科 陕西 西安 710038  
耿倩雯 中国人民解放军联勤保障部队第九八七医院心血管内科 陕西 宝鸡 725000  
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中文摘要:
      摘要 目的:探讨鸢尾素对心肌梗死后大鼠心房颤动和心房间质纤维化的影响。方法:通过结扎左前降支冠状动脉(LADCA)建立急性心肌梗死(MI)大鼠模型,大鼠每天腹腔注射100 μg/kg的鸢尾素1次,共治疗4周。通过超声心动图检查左室舒张末期直径(LVEDD)、左室收缩末期直径(LVESD)、左室射血分数(LVEF)、左室缩短分数(LVFS)。应用苏木精-伊红(HE)染色和Masson三色染色评估大鼠心肌形态和纤维化情况。蛋白质印迹分析检测TGF-β1、Smad2、p-Smad2、Smad3、p-Smad3、MMP9、TIMP-1、collagenⅠ、collagenⅢ、NLRP3、Caspase 1和IL-1β的表达。结果:与模型组相比,鸢尾素组大鼠的LVEF和LVFS升高,而LVEDD和LVESD降低(P<0.05);房颤诱发率和房颤持续时间显著降低(P<0.05);心肌形态明显改善,纤维化面积显著降低(P<0.05);TGFβ1、p-Smad2/3、collagenⅠ、collagenⅢ和MMP9的蛋白表达水平显著降低,TIMP1的蛋白表达水平显著升高(P<0.05);NLRP3炎性体、cleaved-caspase-1和IL-1β的表达水平显著降低(P<0.05)。结论:鸢尾素可显著改善心肌梗死动物模型的心脏功能,抑制心肌纤维化和房颤形成,具有较高的临床应用前景。
英文摘要:
      ABSTRACT Objective: To explore the effects of irisin on atrial fibrillation and interstitial fibrosis in rats after myocardial infarction. Methods: A rat model of acute myocardial infarction (MI) was established by ligation of the left anterior descending coronary artery (LADCA). Rats were intraperitoneally injected with irisin at 100 μg/kg daily for 4 weeks. Left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left ventricular ejection fraction (LVEF), and left ventricular fractional shortening (LVFS) were examined by echocardiography. The rat myocardial morphology and fibrosis were evaluated by hematoxylin-eosin (HE) staining and Masson's trichrome staining. Western blot analysis was used to detect the expression of TGF-β1, Smad2, p-Smad2, Smad3, p-Smad3, MMP9, TIMP-1, collagenⅠ, collagenⅢ, NLRP3, Caspase 1, and IL-1β. Results: Compared with the model group, the LVEF and LVFS of the irisin group were significantly increased, while the LVEDD and LVESD were significantly decreased (P<0.05). The induction rate and duration of atrial fibrillation in the irisin group were significantly reduced (P<0.05). The myocardial morphology of the irisin group was significantly improved, and the fibrosis area was significantly reduced (P<0.05). The protein expression levels of TGFβ1, p-Smad2/3, collagenⅠ, collagenⅢ and MMP9 in the irisin group were significantly reduced, while the protein expression level of TIMP1 was significantly increased (P<0.05). Moreover, the expression levels of NLRP3 inflammasome, cleaved-caspase-1, and IL-1β in irisin group were significantly reduced (P<0.05). Conclusion: Irisin could significantly improve the cardiac function, inhibit the myocardial fibrosis and hypertrophy, and inhibit the formation of atrial fibrillation in an animal model of myocardial infarction. Thus, it has a high clinical application prospect.
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