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[1]吕磊,李瑶,王永园,等.运动预适应减轻一次性运动力竭大鼠心肌凋亡及其机制研究[J].医学研究与战创伤救治(原医学研究生学报),2021,23(03):225-229.[doi:10.3969/j.issn.1672-271X.2021.03.001]
　LV Lei,LI Yao,WANG Yong-yuan,et al.Exercise preconditioning alleviates myocardial apoptosis and its mechanism in rats after exhaustive exercise[J].JOURNAL OF MEDICALRESEARCH —COMBAT TRAUMA CARE,2021,23(03):225-229.[doi:10.3969/j.issn.1672-271X.2021.03.001]
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运动预适应减轻一次性运动力竭大鼠心肌凋亡及其机制研究()
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《医学研究与战创伤救治》（原医学研究生学报）[ISSN:1672-271X/CN:32-1713/R]

卷:
第23卷
期数:
2021年03期
页码:
225-229
栏目:
出版日期:
2021-06-20

文章信息/Info

Title:
Exercise preconditioning alleviates myocardial apoptosis and its mechanism in rats after exhaustive exercise
作者:
吕磊; 李瑶; 王永园; 金涛; 钟勇
作者单位：210002南京，东部战区总医院（原南京军区南京总医院）干部心内科（吕磊、李瑶、王永园），健康医学科（金涛、钟勇）
Author(s):
LV Lei; LI Yao; WANG Yong-yuan; JIN Tao; ZHONG Yong
(1.Department of Geriatric Cardiology, 2.Department of Health Medicine, General Hospital of Eastern Theater Command, PLA, Nanjing 210002，Jiangsu, China）
关键词:
运动预适应; 力竭运动; 凋亡; 内皮型一氧化氮合酶
Keywords:
exercise preconditioning;  exhaustive exercise;  apoptosis;  endothelial nitric oxide synthase
分类号:
R541
DOI:
10.3969/j.issn.1672-271X.2021.03.001
文献标志码:
A
摘要:
目的观察运动预适应对一次性运动力竭大鼠氧化应激水平、心肌细胞凋亡和内皮型一氧化氮合酶（eNOS）的影响，初步探讨其相关作用。 方法建立一次性力竭运动模型，雄性SD大鼠采用随机数字表法分成3组：安静对照组（不运动）、运动力竭组（持续运动直至力竭）和运动预适应组（大鼠在跑台上进行重复4次的间歇性运动），每组7只。HE染色观察光镜下大鼠的心肌组织改变，检测大鼠血清超氧化物歧化酶（SOD）活性、丙二醛（MDA）和一氧化氮（NO）含量。TUNEL染色法检测各组大鼠心肌细胞凋亡，Western blot法检测大鼠心肌内皮型一氧化氮合酶（eNOS）的表达水平。结果光镜下运动力竭组大鼠心肌细胞染色不均匀、排列紊乱，部分肌纤维局限性间质水肿，运动预适应组程度较轻。运动力竭运动组SOD活性[(402.88±53.94)U/mL]较安静对照组[(528.81±76.98) U/mL]低，MDA水平[(11.34±2.44)nmol/mL]较安静对照组[(4.68±0.41) nmol/mL]明显升高，NO含量[(0.05±0.02)μmol/L]较安静对照组[(0.20±0.04) μmol/L]显著降低；运动力竭组凋亡指数为(12.48±2.88)％，与运动力竭组比较，运动预适应组心肌细胞凋亡指数[(3.51±0.78)％]明显降低，SOD活性[(477.43±36.50)U/mL]增加，MDA水平[(7.06±1.89)nmol/mL]降低，NO含量[(0.10±0.02)μmol/L]增加,差异均有统计学意义（P<0.05）。运动力竭组心肌eNOS蛋白表达[（0.56±0.17）]较安静对照组[（1.00±0.12）]下降，而运动预适应组[（1.91±0.22）]显著高于运动力竭组，差异均有统计学意义（P<0.05）。结论运动预适应能减轻一次性力竭运动大鼠心肌损伤所致心肌细胞凋亡和自由基释放，eNOS可能参与这一保护作用。
Abstract:
ObjectiveTo observe the effects of exercise preconditioning on oxidative stress and apoptosis of cardiomyocytes in rats with one-off exhaustion and to explore its possible mechanism.MethodsTwenty one male Sprague Dawley rats were randomly divided into quiet control group, exhaustive exercise group and exercise preconditioning group. The pathological damage of myocardial tissue was observed by hematoxlin-eosin(HE) staining. The activity of serum superoxide dismutase (SOD), the content of malondialdehyde (MDA) and nitric oxide (NO) were detected. Cardiomyocyte apoptosis was detected by terminal deoxyribonucleotide transferase mediated nick end labeling (TUNEL) and the expression of endothelial nitric oxide synthase (eNOS) was detected by Westernblot.ResultsUnder a light microscope, the myocardial cells of exhausted exercise group were arranged disorderly and stained unevenly. Some muscle fibers were arranged disorderly and localized interstitial edema. The degree of myocardial tissue damage in exercise preconditioning group was lighter. Compared with the quiet control group, the activity of SOD in exhaustive exercise group was decreased [(402.88±53.94)U/mL vs (528.81±76.98)U/mL], the level of MDA was significantly increased [(11.34±2.44)nmol/mL vs (4.68±0.41)nmol/mL], and the content of NO was decreased [(0.05±0.02)μmol/L vs (0.20±0.04)μmol/L] (P<0.05). Exercise preconditioning significantly decreased the apoptosis index of myocardial cells [(3.51±0.78)％ vs (12.48±2.88)％ in exhaustive exercise group], increased the activity of SOD[(477.43±36.50)U/mL] and the content of NO [(0.10±0.02)μmol/L], decreased the level of MDA [(7.06±1.89)nmol/mL](P<0.05). The expression of eNOS in exhausted exercise group (0.56±0.17) was lower than that in quiet control group (1.00±0.12) and exercise preconditioning significantly increased the expression of eNOS (1.91±0.22, P＜0.05).ConclusionExercise preconditioning can reduce myocardial cell apoptosis and free radical release induced by one-off exhaustive exercise in rats. eNOS may be involved in this protective effect.

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备注/Memo

备注/Memo:
基金项目：军委后勤保障部卫生局保健专项课题（18BJZ13）；中国博士后科学基金（2018M633765）
更新日期/Last Update: 2021-06-17