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热水浴对慢性应激心肌损伤的防护作用
引用本文:田沛,徐莉,王化宁,王鹏莉,杨红燕,胡文东,邢文娟,高峰. 热水浴对慢性应激心肌损伤的防护作用[J]. 心脏杂志, 2019, 31(3): 260-265. DOI: 10.12125/j.chj.201810034
作者姓名:田沛  徐莉  王化宁  王鹏莉  杨红燕  胡文东  邢文娟  高峰
作者单位:1.航空航天医学系飞行员疗养与康复教研室 空军军医大学
基金项目:国家自然科学基金项目资助(81700342);陕西省高校科协青年人才托举计划项目资助(20180302);军队重大项目资助(AWS16J018);空军后勤重点项目资助(BKJ16R008);空军军医大学军事医学提升计划项目资助(2018HKTS08)
摘    要:目的观察热水浴对应激性心肌损伤的防护作用。方法将18只成年雄性SD大鼠随机分为对照组、应激组和热水浴干预组(简称水浴组),每组6只。利用4周噪声复合足底电击刺激(4 h/d)构建慢性应激损伤模型;热水浴温度为38~40℃。测量大鼠体质量、血压和心脏功能,4周后检测血清应激激素去甲肾上腺素(NE)、血管紧张素(Ang)Ⅱ和心肌酶肌酸激酶(CK)、乳酸脱氢酶(LDH)水平,免疫荧光和Western blot观察组织蛋白,电镜观察心肌线粒体结构。结果与对照组大鼠相比,应激组大鼠存在明显应激反应和心肌损伤,表现为NE、Ang Ⅱ浓度和CK、LDH水平升高(P<0.05);心肌组织自噬相关蛋白LC3B阳性染色和LC3Ⅱ/Ⅰ、p62、Beclin1表达水平增加(P<0.05);线粒体数量减少并呈现结构紊乱。与应激组大鼠相比,热水浴组大鼠NE、Ang Ⅱ浓度和CK、LDH水平降低, p62和Beclin1水平减少(P<0.05),线粒体结构损伤亦有所逆转。结论热水浴能减轻慢性应激状态,调控应激所致心肌细胞自噬紊乱,促进线粒体结构恢复,减轻慢性应激性心肌损伤,其机制有待于进一步研究确认。

关 键 词:应激  心肌损伤  水疗法  线粒体  自噬
收稿时间:2018-10-15

Protective effect of hydrotherapy against chronic stress induced myocardial injury
TIAN Pei,XU Li,WANG Hua-ning,WANG Peng-li,YANG Hong-yan,HU Wen-dong,XING Wen-juan,GAO Feng. Protective effect of hydrotherapy against chronic stress induced myocardial injury[J]. Chinese Heart Journal, 2019, 31(3): 260-265. DOI: 10.12125/j.chj.201810034
Authors:TIAN Pei  XU Li  WANG Hua-ning  WANG Peng-li  YANG Hong-yan  HU Wen-dong  XING Wen-juan  GAO Feng
Affiliation:1.Department of Aerospace Kurortology and rehabilitation, School of Aerospace Medicine Department of Aerospace Kurortology and rehabilitation, School of Aerospace Medicine2.Department of Psychosomatic Medicine, Xijing Hospital3.Department of Aerospace Medical Equipment, Fourth Military Medical University, Xi’an 710032, Shaanxi, China
Abstract: AIM To observe the protective effect of hot water bath (hydrotherapy) on stress induced myocardial injury. METHODS Eighteen adult male Sprague-Dawley rats were randomly divided into control group, stress group and post-stress hot water bath intervention group (water bath group). Rats in the stress group and the water bath (WB) group were subjected to a 4-weeks foot electric shock combined with noise (4 h/d) and the rats in the WB group were given hot bath intervention (38-40 ℃). Body weight, blood pressure and cardiac functions were measured during the experiment and serum stress hormones and myocardial enzymes were measured after 4 weeks. Myocardial protein was determined by immunofluorescence and Western Blot, and the structure of myocardial mitochondria was observed by electron microscope. RESULTS The concentrations of NE and AngII in the serum of rats in the stress group were higher than those in the control group (P<0.05) and the levels of CK and LDH in the stress group increased (P<0.05). Further, compared with those in the control group, the positive staining of microtubule-associated protein 1 light chain 3B (LC3B) and the expressions of LC3II/I, p62 and Beclin1 in myocardial tissue in the stress group increased (P<0.05). Mitochondria showed decreased number and structural disorder in the stress group. Importantly, the hot water bath intervention decreased serum NE, Ang II concentrations and CK and LDH levels compared with those in the stress group (P<0.05). In addition, hot water bath significantly decreased p62 and Beclin1 expression levels (P<0.05) and reversed the mitochondrial structural damage. CONCLUSION Hot water bath reduce myocardial autophagy, improves mitochondrial structure and alleviates chronic stress induced myocardial injury where the mechanisms need further studies.
Keywords:stress  myocardial injury  hydrotherapy  mitochondria  autophagyQidantongmai
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