中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
2期
270-272
,共3页
田轶魁%付强%董福强%杜鑫%芦志红%魏民新
田軼魁%付彊%董福彊%杜鑫%蘆誌紅%魏民新
전질괴%부강%동복강%두흠%호지홍%위민신
miRNA-133a%心肌缺血%再灌注损伤%心脏功能
miRNA-133a%心肌缺血%再灌註損傷%心髒功能
miRNA-133a%심기결혈%재관주손상%심장공능
MicroRNA-133a%Myocardial ischemia%Reperfusion injury%Cardiac function
目的 观察上调miRNA-133a表达是否可改善缺血再灌注损伤后心肌损害及心脏功能.方法 建立活体大鼠心肌缺血再灌注损伤模型.将实验动物随机分为5组:(1)空白对照组(Sham组)；(2)缺血再灌注损伤组(I/R组)；(3)缺血再灌注损伤+miRNA-133a模拟物agomiR-133a组(I/R+ agomiR-133a组)；(4)缺血再灌注损伤+阴性对照序列组(I/R+ scramble组)；(5)缺血再灌注损伤组+生理盐水组(I/R+ NS组).于再灌注24h分别使用实时定量聚合酶链反应(Real-TimePCR)法检查心肌内miRNA-133a表达水平；经胸超声心动检查大鼠心脏功能；2,3,5-氯化三苯基四氮唑(TTC)染色检测心肌梗死以及TdT介导的dUTP缺口末端标记(TUNEL)检测心肌细胞凋亡.结果 I/R+ agomiR-133a组心肌内miRNA表达水平显著高于I/R组(P＜0.01).上调miRNA-133a表达水平可显著减少再灌注后心肌梗死面积[(37.0±3.1)％比(58.0±4.4)％,P＜0.01],抑制心肌细胞凋亡(38.4±6.0比15.7±5.2,P＜0.01),并改善心脏功能[LVEF:(64.8 ±2.9)％比(52.8±4.0)％,LVFS:(31.1±1.2)％比(25.2±0.8)％,P＜0.01].NS与scramble对再灌注后心肌损伤及心脏功能无显著影响.结论 上调心肌内miRNA-133a表达水平可显著减轻缺血再灌注损伤24h后心肌损害,并改善心脏功能.
目的 觀察上調miRNA-133a錶達是否可改善缺血再灌註損傷後心肌損害及心髒功能.方法 建立活體大鼠心肌缺血再灌註損傷模型.將實驗動物隨機分為5組:(1)空白對照組(Sham組)；(2)缺血再灌註損傷組(I/R組)；(3)缺血再灌註損傷+miRNA-133a模擬物agomiR-133a組(I/R+ agomiR-133a組)；(4)缺血再灌註損傷+陰性對照序列組(I/R+ scramble組)；(5)缺血再灌註損傷組+生理鹽水組(I/R+ NS組).于再灌註24h分彆使用實時定量聚閤酶鏈反應(Real-TimePCR)法檢查心肌內miRNA-133a錶達水平；經胸超聲心動檢查大鼠心髒功能；2,3,5-氯化三苯基四氮唑(TTC)染色檢測心肌梗死以及TdT介導的dUTP缺口末耑標記(TUNEL)檢測心肌細胞凋亡.結果 I/R+ agomiR-133a組心肌內miRNA錶達水平顯著高于I/R組(P＜0.01).上調miRNA-133a錶達水平可顯著減少再灌註後心肌梗死麵積[(37.0±3.1)％比(58.0±4.4)％,P＜0.01],抑製心肌細胞凋亡(38.4±6.0比15.7±5.2,P＜0.01),併改善心髒功能[LVEF:(64.8 ±2.9)％比(52.8±4.0)％,LVFS:(31.1±1.2)％比(25.2±0.8)％,P＜0.01].NS與scramble對再灌註後心肌損傷及心髒功能無顯著影響.結論 上調心肌內miRNA-133a錶達水平可顯著減輕缺血再灌註損傷24h後心肌損害,併改善心髒功能.
목적 관찰상조miRNA-133a표체시부가개선결혈재관주손상후심기손해급심장공능.방법 건립활체대서심기결혈재관주손상모형.장실험동물수궤분위5조:(1)공백대조조(Sham조)；(2)결혈재관주손상조(I/R조)；(3)결혈재관주손상+miRNA-133a모의물agomiR-133a조(I/R+ agomiR-133a조)；(4)결혈재관주손상+음성대조서렬조(I/R+ scramble조)；(5)결혈재관주손상조+생리염수조(I/R+ NS조).우재관주24h분별사용실시정량취합매련반응(Real-TimePCR)법검사심기내miRNA-133a표체수평；경흉초성심동검사대서심장공능；2,3,5-록화삼분기사담서(TTC)염색검측심기경사이급TdT개도적dUTP결구말단표기(TUNEL)검측심기세포조망.결과 I/R+ agomiR-133a조심기내miRNA표체수평현저고우I/R조(P＜0.01).상조miRNA-133a표체수평가현저감소재관주후심기경사면적[(37.0±3.1)％비(58.0±4.4)％,P＜0.01],억제심기세포조망(38.4±6.0비15.7±5.2,P＜0.01),병개선심장공능[LVEF:(64.8 ±2.9)％비(52.8±4.0)％,LVFS:(31.1±1.2)％비(25.2±0.8)％,P＜0.01].NS여scramble대재관주후심기손상급심장공능무현저영향.결론 상조심기내miRNA-133a표체수평가현저감경결혈재관주손상24h후심기손해,병개선심장공능.
Objective To evaluate the protective roles of miRNA-133a against myocardial ischemia-reperfusion (I/R) injury.Methods Healthy adult male Wistar rats were divided into five groups:( 1 ) Sham group,(2) I/R group,(3) I/R + agomiR-133a group,(4) I/R + scramble group and I/R +NS group.Cardiac function was analyzed by echocardiography 24 h after reperfusion.miRNA-133a levels were detected by real-time polymerase chain reaction (qRT-PCR).Myocardial infarction size was analyzed by the tovanto transit commission (TTC) staining.TdT-mediated dUTP nick end labeling (TUNEL) staining was used to detect myocardial apoptosis.Results AgomiR-133a significantly increased myocardial miRNA-133a levels ( P ＜ 0.01 ),reduced infarction size [ ( 37.0 ± 3.1 ) ％ vs ( 58.0 ± 4.4 ) ％,P ＜0.01 ],inhibited myocardial apoptosis (38.4 ±6.0 vs 15.7 ±5.2,P ＜0.01 ) and improved cardiac function [LVEF:(64.8 ±2.9)％ vs (52.8±4.0)％,LVFS:(31.1 ±1.2)％ vs (25.2 ±0.8)％,P＜0.01 ] 24 h after reperfusion.Conclusion Up-regulation myocardial miRNA-133a levels using agomiR133a reduced myocardial I/R injury and improved cardiac function.
