体育科学
體育科學
체육과학
China Sport Science
2015年
5期
55~61
,共null页
M3受体 MEK1/2-ERK1/2通路 心肌细胞凋亡 持续有氧运动 高强度间歇运动 心肌梗死
M3受體 MEK1/2-ERK1/2通路 心肌細胞凋亡 持續有氧運動 高彊度間歇運動 心肌梗死
M3수체 MEK1/2-ERK1/2통로 심기세포조망 지속유양운동 고강도간헐운동 심기경사
M3 receptor （M3R ） ; MEK1/2 -ERK 1/2 signaling pathways ; cardiomyocyte apoptosis; aerobic exercise; high-intensity interval exercise ; myocardial infarction
目的：探讨运动上调M3受体（M3R）对心肌梗死（MI）大鼠心脏产生保护效应及其机制。方法：雄性SD大鼠48只,随机分为正常对照组（C）,心梗组（MI）,心梗＋中强度持续有氧运动组（ME1）,心梗＋高强度间歇运动组（ME2）,每组12只。C组常规饲养,MI组采用左冠脉前降支结扎法（LAD）建立MI模型。ME1和ME2组心梗手术1周后进行跑台运动,60min/次,1次/d,5d/1周×8周。ME1组以10m/min×5min,再以3m/min速度递增至16m/min。ME2组以10m/min×10 min后,逐渐递增至25 m/min×7 min;之后以15 m/min×3min间歇运动,依次交替进行。训练结束后次日,腹腔麻醉进行颈动脉插管测定LVSP、LVEDP、±dp/dtmax等指标,评定心功能变化。之后迅速开胸摘取心脏,分别进行组织学制片、Masson染色观察心肌胶原纤维变化,免疫荧光法观察分析心肌M3R表达,Western Blot法检测心肌M3R、MEK1/2、p-ERK1/2、ERK1/2、Bcl-2和Bax蛋白表达。结果：MI组胶原容积百分比（CVF%）和LVEDP较C组显著升高（P〈0.01）,LVSP和±dp/dtmax较C组均显著降低（P〈0.01）。MI后可见心肌M3R阳性染色,且M3R、MEK1/2、p-ERK1/2/ERK1/2表达较C组均显著升高（P〈0.01）,Bcl-2/Bax比值较C组显著降低（P〈0.01）。ME1和ME2组CVF%和LVEDP较MI组均显著降低（P〈0.01）,ME1组-dP/dt max较MI组显著升高（P〈0.01）,ME2组LVSP较MI组显著升高（P〈0.01）。ME1和ME2组均可见心肌M3R阳性染色,M3R、MEK1/2、p-ERK1/2/ERK1/2表达较MI组显著增加（P〈0.01）,Bcl-2/Bax比值较MI组显著升高（P〈0.01,P〈0.05）,ME1组和ME2组间无显著差异。结论：持续有氧运动和高强度间歇运动均可上调心梗心肌M3R-MEK1/2-ERK1/2通路,抑制心肌细胞凋亡,改善心肌纤维化程度,保护心梗大鼠心功能。心梗心肌M3R-MEK1/2-ERK1/2-细胞凋亡途径与持续和间歇运动方式及运动强度关系不密切。
目的：探討運動上調M3受體（M3R）對心肌梗死（MI）大鼠心髒產生保護效應及其機製。方法：雄性SD大鼠48隻,隨機分為正常對照組（C）,心梗組（MI）,心梗＋中彊度持續有氧運動組（ME1）,心梗＋高彊度間歇運動組（ME2）,每組12隻。C組常規飼養,MI組採用左冠脈前降支結扎法（LAD）建立MI模型。ME1和ME2組心梗手術1週後進行跑檯運動,60min/次,1次/d,5d/1週×8週。ME1組以10m/min×5min,再以3m/min速度遞增至16m/min。ME2組以10m/min×10 min後,逐漸遞增至25 m/min×7 min;之後以15 m/min×3min間歇運動,依次交替進行。訓練結束後次日,腹腔痳醉進行頸動脈插管測定LVSP、LVEDP、±dp/dtmax等指標,評定心功能變化。之後迅速開胸摘取心髒,分彆進行組織學製片、Masson染色觀察心肌膠原纖維變化,免疫熒光法觀察分析心肌M3R錶達,Western Blot法檢測心肌M3R、MEK1/2、p-ERK1/2、ERK1/2、Bcl-2和Bax蛋白錶達。結果：MI組膠原容積百分比（CVF%）和LVEDP較C組顯著升高（P〈0.01）,LVSP和±dp/dtmax較C組均顯著降低（P〈0.01）。MI後可見心肌M3R暘性染色,且M3R、MEK1/2、p-ERK1/2/ERK1/2錶達較C組均顯著升高（P〈0.01）,Bcl-2/Bax比值較C組顯著降低（P〈0.01）。ME1和ME2組CVF%和LVEDP較MI組均顯著降低（P〈0.01）,ME1組-dP/dt max較MI組顯著升高（P〈0.01）,ME2組LVSP較MI組顯著升高（P〈0.01）。ME1和ME2組均可見心肌M3R暘性染色,M3R、MEK1/2、p-ERK1/2/ERK1/2錶達較MI組顯著增加（P〈0.01）,Bcl-2/Bax比值較MI組顯著升高（P〈0.01,P〈0.05）,ME1組和ME2組間無顯著差異。結論：持續有氧運動和高彊度間歇運動均可上調心梗心肌M3R-MEK1/2-ERK1/2通路,抑製心肌細胞凋亡,改善心肌纖維化程度,保護心梗大鼠心功能。心梗心肌M3R-MEK1/2-ERK1/2-細胞凋亡途徑與持續和間歇運動方式及運動彊度關繫不密切。
목적：탐토운동상조M3수체（M3R）대심기경사（MI）대서심장산생보호효응급기궤제。방법：웅성SD대서48지,수궤분위정상대조조（C）,심경조（MI）,심경＋중강도지속유양운동조（ME1）,심경＋고강도간헐운동조（ME2）,매조12지。C조상규사양,MI조채용좌관맥전강지결찰법（LAD）건립MI모형。ME1화ME2조심경수술1주후진행포태운동,60min/차,1차/d,5d/1주×8주。ME1조이10m/min×5min,재이3m/min속도체증지16m/min。ME2조이10m/min×10 min후,축점체증지25 m/min×7 min;지후이15 m/min×3min간헐운동,의차교체진행。훈련결속후차일,복강마취진행경동맥삽관측정LVSP、LVEDP、±dp/dtmax등지표,평정심공능변화。지후신속개흉적취심장,분별진행조직학제편、Masson염색관찰심기효원섬유변화,면역형광법관찰분석심기M3R표체,Western Blot법검측심기M3R、MEK1/2、p-ERK1/2、ERK1/2、Bcl-2화Bax단백표체。결과：MI조효원용적백분비（CVF%）화LVEDP교C조현저승고（P〈0.01）,LVSP화±dp/dtmax교C조균현저강저（P〈0.01）。MI후가견심기M3R양성염색,차M3R、MEK1/2、p-ERK1/2/ERK1/2표체교C조균현저승고（P〈0.01）,Bcl-2/Bax비치교C조현저강저（P〈0.01）。ME1화ME2조CVF%화LVEDP교MI조균현저강저（P〈0.01）,ME1조-dP/dt max교MI조현저승고（P〈0.01）,ME2조LVSP교MI조현저승고（P〈0.01）。ME1화ME2조균가견심기M3R양성염색,M3R、MEK1/2、p-ERK1/2/ERK1/2표체교MI조현저증가（P〈0.01）,Bcl-2/Bax비치교MI조현저승고（P〈0.01,P〈0.05）,ME1조화ME2조간무현저차이。결론：지속유양운동화고강도간헐운동균가상조심경심기M3R-MEK1/2-ERK1/2통로,억제심기세포조망,개선심기섬유화정도,보호심경대서심공능。심경심기M3R-MEK1/2-ERK1/2-세포조망도경여지속화간헐운동방식급운동강도관계불밀절。
objective： Cardioprotective effect and mechanism of exercise training up-regulating the expression of M3 receptor on myocardial infarction. Methods. 48 male Sprague-Dawley rats were randomly assigned to four groups （n= 12, per group） .-control group （C）, myocardial in- farction group （MI）, moderate-intensity aerobic exercise with myocardial infarction group （ME1） and high-intensity aerobic interval exercise with myocardial infarction group （ME2）, Rats in C group are breed normally. MI was induced by ligation of the left anterior descending （LAD） coronary artery in MI group~ Rats in ME1 and ME2 group take treadmill exercise for 8wk after lwk post-operation. ME1 group running began at the speed of 10m/min for 5min, then accelerate from 3m/min to 16m/rain. ME2 group running began at the speed of 10m/ rain for 10min,then the speed increases to 25 m/min, after 7min, slow down at the speed of 15m/min for 3min. Take the process alternatively. The total exercise time of ME1 and ME2 are both 60 min, 5 d/lwk X 8 wk. LVSP, LVEDP, ± dp/dtmax and the cardiac function changes are measured after training. Myocardial collagen fibers were observed by histological section and Masson staining. The expression of myocardial Ma R was observed and analyzed by immun- oflourecence. The myocardial protein content of M3 R, MEK1/2, P-ERK1/2, ERK1/2 and apoptosis related Bcl-2 and Bax were assayed by Western Blot. Results ： MI increased CVF and LV- EDP （P〈0. 01）, but decreased LVSP and -dp/dtmax （P%0. 01）. After MI myocardial M3 positive staining, after MI Ma protein expression significantly higher （ P 〈 0.01 ）, MEK1/2 , P- ERK1/2/ERKI/2 protein expression were significantly increased （P 〈 0. 01, P 〈 0. 01 ）, after the MI the Bcl-2/Bax expression significantly reduced （P 〈 0. 01）. ME1 and ME2 group CVF, LVEDP significantly reduced （P%0.01）, ME1 -dp/dtm~x significantly increased （P 〈 0.01）, ME2 LVSP increased significantly （P 〈0.01）. ME1 and ME2 groups were identified myocardial Ma, ME1 and ME2 Ma protein expression significantly increased （ P 〈 0.01, P 〈. 0.01）. ME1 and ME2 group Bcl-2/Bax expression significantly reduced in the MI group （P d0.01,P%0.01）. ME1 and ME2 index had no significant difference. Conclusions.. Moder- ate-intensity aerobic exercise and high-intensity aerobic interval exercise can upregulate the M3 R-MEK1/2-ERK1/2 signaling pathway, thus inhibit the apoptosis of myocardial cells, reduce myocardial interstitial fibrosis and promote cardiac function after MI.
