体育科学
體育科學
체육과학
China Sport Science
2014年
9期
23~30
,共null页
抗阻训练 心肌梗死 心脏保护 神经调节蛋白1 心肌修复
抗阻訓練 心肌梗死 心髒保護 神經調節蛋白1 心肌脩複
항조훈련 심기경사 심장보호 신경조절단백1 심기수복
resistance training; myocardial infarction; cardioprotection; Neuregulin-1; cardiac repair
目的：探讨抗阻训练对心梗（Myocardial Infarction,MI）大鼠心肌组织中神经调节蛋白（Neuregulin-1,NRG1）及其信号通路表达的影响及其对心脏结构与功能的保护效应。方法：3月龄雄性SD大鼠,体重180~220g,随机分为假手术组（Sham）、心梗组（MI）和心梗抗阻训练组（MR）,每组10只。MI和MR组结扎左冠脉前降支（LAD）,建立MI模型。其中MR组于术后1周进行为期4周的抗阻训练,结束后测定心功能;采用石蜡切片和HE、Masson染色技术观察并计算组织形态学变化和胶原容积分数（Collagen volume fraction,CVF）,采用免疫组化、Real Time-qPCR和Western Blotting技术检测心肌血管新生、细胞凋亡等相关蛋白α-SMA、CD105、BCL-2和Bax以及NRG1及其受体ErbB2/4和下游信号通路蛋白的表达变化。结果：抗阻训练有效提升了MI大鼠心功能,改善心肌细胞病理性肥大;促进非梗死区心肌α-SMA和CD105表达、显著升高BCL-2/Bax比值;显著增加MI大鼠心肌NRG1蛋白的表达和erbb2mRNA表达,升高PI3K-Akt和ERK1/2的磷酸化水平。结论：本研究发现,抗阻训练可改善MI心脏的病理性重塑,促进非梗死区血管新生,抑制心肌细胞凋亡,安全有效的改善MI心脏的功能;抗阻训练可促进心肌NRG1及其ErbBs的表达,其心脏的保护效应与心肌NRG1/ErbBs及PI3K/Akt和ERK1/2信号通路激活有关。
目的：探討抗阻訓練對心梗（Myocardial Infarction,MI）大鼠心肌組織中神經調節蛋白（Neuregulin-1,NRG1）及其信號通路錶達的影響及其對心髒結構與功能的保護效應。方法：3月齡雄性SD大鼠,體重180~220g,隨機分為假手術組（Sham）、心梗組（MI）和心梗抗阻訓練組（MR）,每組10隻。MI和MR組結扎左冠脈前降支（LAD）,建立MI模型。其中MR組于術後1週進行為期4週的抗阻訓練,結束後測定心功能;採用石蠟切片和HE、Masson染色技術觀察併計算組織形態學變化和膠原容積分數（Collagen volume fraction,CVF）,採用免疫組化、Real Time-qPCR和Western Blotting技術檢測心肌血管新生、細胞凋亡等相關蛋白α-SMA、CD105、BCL-2和Bax以及NRG1及其受體ErbB2/4和下遊信號通路蛋白的錶達變化。結果：抗阻訓練有效提升瞭MI大鼠心功能,改善心肌細胞病理性肥大;促進非梗死區心肌α-SMA和CD105錶達、顯著升高BCL-2/Bax比值;顯著增加MI大鼠心肌NRG1蛋白的錶達和erbb2mRNA錶達,升高PI3K-Akt和ERK1/2的燐痠化水平。結論：本研究髮現,抗阻訓練可改善MI心髒的病理性重塑,促進非梗死區血管新生,抑製心肌細胞凋亡,安全有效的改善MI心髒的功能;抗阻訓練可促進心肌NRG1及其ErbBs的錶達,其心髒的保護效應與心肌NRG1/ErbBs及PI3K/Akt和ERK1/2信號通路激活有關。
목적：탐토항조훈련대심경（Myocardial Infarction,MI）대서심기조직중신경조절단백（Neuregulin-1,NRG1）급기신호통로표체적영향급기대심장결구여공능적보호효응。방법：3월령웅성SD대서,체중180~220g,수궤분위가수술조（Sham）、심경조（MI）화심경항조훈련조（MR）,매조10지。MI화MR조결찰좌관맥전강지（LAD）,건립MI모형。기중MR조우술후1주진행위기4주적항조훈련,결속후측정심공능;채용석사절편화HE、Masson염색기술관찰병계산조직형태학변화화효원용적분수（Collagen volume fraction,CVF）,채용면역조화、Real Time-qPCR화Western Blotting기술검측심기혈관신생、세포조망등상관단백α-SMA、CD105、BCL-2화Bax이급NRG1급기수체ErbB2/4화하유신호통로단백적표체변화。결과：항조훈련유효제승료MI대서심공능,개선심기세포병이성비대;촉진비경사구심기α-SMA화CD105표체、현저승고BCL-2/Bax비치;현저증가MI대서심기NRG1단백적표체화erbb2mRNA표체,승고PI3K-Akt화ERK1/2적린산화수평。결론：본연구발현,항조훈련가개선MI심장적병이성중소,촉진비경사구혈관신생,억제심기세포조망,안전유효적개선MI심장적공능;항조훈련가촉진심기NRG1급기ErbBs적표체,기심장적보호효응여심기NRG1/ErbBs급PI3K/Akt화ERK1/2신호통로격활유관。
Objectives：To discuss the influence of resistance training on cardiac structure and function,expression of Neuregulin-1（NRG1）and its signaling pathway in rats with myocardial infarction（MI）.Methods：Adult male sprague-dawley rats,3-mouth old,weight about 180-220 g were randomly divided into three groups：Sham-operated group（Sham）,sedentary MI group（MI）and MI with resistance training group（MR）.The MI model in rat was established by ligation of the left anterior descending（LAD）coronary artery,and rats in MR were subjected to 4-week resistance training.At the end of the 4-week training,hemodynamic measurement was preformed to evaluate cardiac function;after that the heart was picked for histological section.The expression levels ofα-SMA,CD105,BCL-2,Bax,NRG1,ErbB2,ErbB4,PI3 K,Akt and ERK1/2were detected by Immunohistochemical measurement,Western Blotting or RT-qPCR.Results：Compared with MI group,resistance training has effectively promoted cardiac function and the pathological myocardial hypertrophy,increased BCL-2/Bax ratio and the expression ofα-SMA,CD105,NRG1 protein and erbb2,erbb4 mRNA in myocardial tissue,upregulated the phosphorylation levels of PI3K-Akt and ERK1/2 signal.Conclusion：Resistance training could improve the cardiac function by ameliorating cardiomyocyte pathologic hypertrophy,inhibiting apoptosis and promoting angiogenesis after MI,its mechanism may be associated with NRG1 and the activation of its downstream signaling pathways.
