中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2009年
3期
274-276
,共3页
杨运海%韩召敏%李伟栋%屠政良%倪一鸣
楊運海%韓召敏%李偉棟%屠政良%倪一鳴
양운해%한소민%리위동%도정량%예일명
3-NPA%缺血-再灌注%细胞凋亡%心肌
3-NPA%缺血-再灌註%細胞凋亡%心肌
3-NPA%결혈-재관주%세포조망%심기
3-nitropropionic acid%Ischemia-reperfusion%Apoptosis%Myocardium
目的 观察三硝基丙酸(3-NPA)预处理对缺血-再灌注兔心肌细胞凋亡的影响及其机制.方法 24只新两兰大耳兔随机分为对照组(C组)、实验组(3-NPA组)和阻滞剂组(5-HD)组),每组8只.5-HD组在开胸前24 h通过耳缘静脉注射特异性线粒体NIP敏感钾通道阻滞剂5-羟基癸酸(5 mg·kg-1),C组和3-NPA组注射同样体积的生理盐水.10 min后3-NPA组和5-HD组注射3-硝基丙酸(3mg·kg-1),C组注射同样体积的生理盐水.通过结扎兔左冠状动脉建立心肌缺血-再灌注动物模型,三组缺血 30 min再灌注120 min.检测再灌注120 min后心肌梗死面积、心肌细胞凋亡指数、Bcl-2和Bax蛋白的表达.对实验数据进行方差分析榆验.结果 3-NPA组的心肌梗死面积显著低于其它C组[(0.26±0.07)vs.(0.45±0.09),P＜0.01]和5-HD组[(0.26±0.07)vs.(0.40±0.07),P＜0.01];C组和5-HD组之间没有显著性差异[(0.45±0.09)vs.(0.40±0.07),P＞0.05].3-NPA组心肌细胞凋亡指数明显小于C组[(27.72±5.18)vs.(45.91±10.54),P＜0.01]和5-HD组[(27.72±5.18)vs.(43.44±7.33),P＜0.01].3-NPA组bcl-2表达高于另外两组[(0.123±0.046)vs.(0.079±0.019),(0.080±0.019),P＜0.05],而Bax明显低于另外两组[(0.095±0.020)vs.(0.14±0.05) and(0.15±0.05),P＜0.05].结论 3-NPA预处理对缺血-再灌注心肌具有良好的扰凋亡作用,这与其开放断线粒体ATP敏感钾通道有关.
目的 觀察三硝基丙痠(3-NPA)預處理對缺血-再灌註兔心肌細胞凋亡的影響及其機製.方法 24隻新兩蘭大耳兔隨機分為對照組(C組)、實驗組(3-NPA組)和阻滯劑組(5-HD)組),每組8隻.5-HD組在開胸前24 h通過耳緣靜脈註射特異性線粒體NIP敏感鉀通道阻滯劑5-羥基癸痠(5 mg·kg-1),C組和3-NPA組註射同樣體積的生理鹽水.10 min後3-NPA組和5-HD組註射3-硝基丙痠(3mg·kg-1),C組註射同樣體積的生理鹽水.通過結扎兔左冠狀動脈建立心肌缺血-再灌註動物模型,三組缺血 30 min再灌註120 min.檢測再灌註120 min後心肌梗死麵積、心肌細胞凋亡指數、Bcl-2和Bax蛋白的錶達.對實驗數據進行方差分析榆驗.結果 3-NPA組的心肌梗死麵積顯著低于其它C組[(0.26±0.07)vs.(0.45±0.09),P＜0.01]和5-HD組[(0.26±0.07)vs.(0.40±0.07),P＜0.01];C組和5-HD組之間沒有顯著性差異[(0.45±0.09)vs.(0.40±0.07),P＞0.05].3-NPA組心肌細胞凋亡指數明顯小于C組[(27.72±5.18)vs.(45.91±10.54),P＜0.01]和5-HD組[(27.72±5.18)vs.(43.44±7.33),P＜0.01].3-NPA組bcl-2錶達高于另外兩組[(0.123±0.046)vs.(0.079±0.019),(0.080±0.019),P＜0.05],而Bax明顯低于另外兩組[(0.095±0.020)vs.(0.14±0.05) and(0.15±0.05),P＜0.05].結論 3-NPA預處理對缺血-再灌註心肌具有良好的擾凋亡作用,這與其開放斷線粒體ATP敏感鉀通道有關.
목적 관찰삼초기병산(3-NPA)예처리대결혈-재관주토심기세포조망적영향급기궤제.방법 24지신량란대이토수궤분위대조조(C조)、실험조(3-NPA조)화조체제조(5-HD)조),매조8지.5-HD조재개흉전24 h통과이연정맥주사특이성선립체NIP민감갑통도조체제5-간기계산(5 mg·kg-1),C조화3-NPA조주사동양체적적생리염수.10 min후3-NPA조화5-HD조주사3-초기병산(3mg·kg-1),C조주사동양체적적생리염수.통과결찰토좌관상동맥건립심기결혈-재관주동물모형,삼조결혈 30 min재관주120 min.검측재관주120 min후심기경사면적、심기세포조망지수、Bcl-2화Bax단백적표체.대실험수거진행방차분석유험.결과 3-NPA조적심기경사면적현저저우기타C조[(0.26±0.07)vs.(0.45±0.09),P＜0.01]화5-HD조[(0.26±0.07)vs.(0.40±0.07),P＜0.01];C조화5-HD조지간몰유현저성차이[(0.45±0.09)vs.(0.40±0.07),P＞0.05].3-NPA조심기세포조망지수명현소우C조[(27.72±5.18)vs.(45.91±10.54),P＜0.01]화5-HD조[(27.72±5.18)vs.(43.44±7.33),P＜0.01].3-NPA조bcl-2표체고우령외량조[(0.123±0.046)vs.(0.079±0.019),(0.080±0.019),P＜0.05],이Bax명현저우령외량조[(0.095±0.020)vs.(0.14±0.05) and(0.15±0.05),P＜0.05].결론 3-NPA예처리대결혈-재관주심기구유량호적우조망작용,저여기개방단선립체ATP민감갑통도유관.
Objective To investigate the effects of preconditioning with 3-nitropropionie acid on myocardial apoptosis induced by ischemia-reperfusion injury.Method Twenty-four rabbits were randomly divided into control group(group C,n=8),precondition group(group 3-NPA,n=8)and 5-HD group(group 5-HD,n=8).The group 5-HD was treated intravenously with 5 mg·kg-1 5-HD(ATP-sensitive potassium channels blocker),group C and group 3-NPA received normal saline instead of 5-HD.Ten minutes later,5-HD group and 3-NPA group were injected with 3-NPA(3 mg·kg-1)and the group C was injected with normal saline.Twenty-four hours later,the left anterior descending coronary artery was ligated for 30 min and then unclamped for 120 min to estabhsh ischemi-a-reperfitsion injury model.After reperfusion,the infarct sizes of ventricular myocardium,apoptotic myocardial cells and the expressions of Bcl-2 and Bax protein were measured.Results Infarct sizes and apoptotic myocardial cells in group 3-NPA were less than those in the others(P＜0.01).The expressions of Bcl-2 in group 3-NPA.in-creased as compared with group C(P＜0.05)and group 5-HD(P＜0.05),whereas the expressions of Bax in group 3-NPA decreased as compared with group C(P＜0.05)and group 5-HD(P＜0.05).Conclusions Preconditioning with 3-nitmpropionie acid reduces myocardial apoptosis induced by isehemia-reporfusion injury which is attributed to the opening of mitochondrial KATP channels.
