中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2014年
2期
147-150
,共4页
朱宁%张喆%于哲%孙贺英%董自平
硃寧%張喆%于哲%孫賀英%董自平
주저%장철%우철%손하영%동자평
缺血预适应%糖尿病%心肌缺血/再灌注%细胞凋亡%大鼠
缺血預適應%糖尿病%心肌缺血/再灌註%細胞凋亡%大鼠
결혈예괄응%당뇨병%심기결혈/재관주%세포조망%대서
Ischemic preconditioning%Diabetes mellitus%Myocardial ischemia/reperfusion%Apoptosis%Rat
目的 探讨缺血预适应对糖尿病大鼠心肌缺血/再灌注损伤的保护效应.方法 健康雄性大鼠28只,尾静脉注射链脲佐菌素45 mg/kg制备糖尿病大鼠模型,普通饲料喂养4周后随机分为缺血/再灌注(I/R)组和缺血预适应(IP)组.观察两组大鼠缺血前和缺血即刻、缺血15 min、缺血30 min以及再灌注30 min、再灌注2h心电图ST段改变及室性心律失常的发生情况,TTC染色评价心肌细胞坏死情况,TUNEL法检测心肌细胞凋亡情况,免疫组织化学染色法检测心肌组织凋亡相关基因Bcl-2与Bax蛋白表达情况.结果 与I/R组比较,IP组缺血30 min时ST段抬高幅度明显降低[(0.675±0.150)、(0.489±0.161) mV,P＜0.05],室性期前收缩出现时间推迟[(6.47±4.28)、(18.21±5.36) min,t=5.241,P=0.000],室性期前收缩持续时间缩短[(16.71±5.48)、(6.07±4.33) min,t=4.924,P=0.002],室性心动过速、心室颤动发生率显著下降[57.14％ (8/14)与14.29％ (2/14),x2=5.600,P=0.018;50.00％(7/14)与14.29％(2/14),x2=4.094,P=0.043],心肌梗死范围缩小[(37.50±11.40)％、(12.50±9.45)％,t=3.211,P=0.006],凋亡指数亦降低[(24.31±3.12)％、(19.01±4.32)％,t=3.227,P=0.006],并伴有凋亡相关蛋白Bcl-2/Bax上调(0.103±0.045、0.221±0.101,t=2.670,P=0.015).结论 缺血预适应对病程4周糖尿病大鼠心肌缺血/再灌注损伤具有保护效应,其通过上调凋亡相关基因Bcl-2/Bax,减少心肌细胞凋亡.
目的 探討缺血預適應對糖尿病大鼠心肌缺血/再灌註損傷的保護效應.方法 健康雄性大鼠28隻,尾靜脈註射鏈脲佐菌素45 mg/kg製備糖尿病大鼠模型,普通飼料餵養4週後隨機分為缺血/再灌註(I/R)組和缺血預適應(IP)組.觀察兩組大鼠缺血前和缺血即刻、缺血15 min、缺血30 min以及再灌註30 min、再灌註2h心電圖ST段改變及室性心律失常的髮生情況,TTC染色評價心肌細胞壞死情況,TUNEL法檢測心肌細胞凋亡情況,免疫組織化學染色法檢測心肌組織凋亡相關基因Bcl-2與Bax蛋白錶達情況.結果 與I/R組比較,IP組缺血30 min時ST段抬高幅度明顯降低[(0.675±0.150)、(0.489±0.161) mV,P＜0.05],室性期前收縮齣現時間推遲[(6.47±4.28)、(18.21±5.36) min,t=5.241,P=0.000],室性期前收縮持續時間縮短[(16.71±5.48)、(6.07±4.33) min,t=4.924,P=0.002],室性心動過速、心室顫動髮生率顯著下降[57.14％ (8/14)與14.29％ (2/14),x2=5.600,P=0.018;50.00％(7/14)與14.29％(2/14),x2=4.094,P=0.043],心肌梗死範圍縮小[(37.50±11.40)％、(12.50±9.45)％,t=3.211,P=0.006],凋亡指數亦降低[(24.31±3.12)％、(19.01±4.32)％,t=3.227,P=0.006],併伴有凋亡相關蛋白Bcl-2/Bax上調(0.103±0.045、0.221±0.101,t=2.670,P=0.015).結論 缺血預適應對病程4週糖尿病大鼠心肌缺血/再灌註損傷具有保護效應,其通過上調凋亡相關基因Bcl-2/Bax,減少心肌細胞凋亡.
목적 탐토결혈예괄응대당뇨병대서심기결혈/재관주손상적보호효응.방법 건강웅성대서28지,미정맥주사련뇨좌균소45 mg/kg제비당뇨병대서모형,보통사료위양4주후수궤분위결혈/재관주(I/R)조화결혈예괄응(IP)조.관찰량조대서결혈전화결혈즉각、결혈15 min、결혈30 min이급재관주30 min、재관주2h심전도ST단개변급실성심률실상적발생정황,TTC염색평개심기세포배사정황,TUNEL법검측심기세포조망정황,면역조직화학염색법검측심기조직조망상관기인Bcl-2여Bax단백표체정황.결과 여I/R조비교,IP조결혈30 min시ST단태고폭도명현강저[(0.675±0.150)、(0.489±0.161) mV,P＜0.05],실성기전수축출현시간추지[(6.47±4.28)、(18.21±5.36) min,t=5.241,P=0.000],실성기전수축지속시간축단[(16.71±5.48)、(6.07±4.33) min,t=4.924,P=0.002],실성심동과속、심실전동발생솔현저하강[57.14％ (8/14)여14.29％ (2/14),x2=5.600,P=0.018;50.00％(7/14)여14.29％(2/14),x2=4.094,P=0.043],심기경사범위축소[(37.50±11.40)％、(12.50±9.45)％,t=3.211,P=0.006],조망지수역강저[(24.31±3.12)％、(19.01±4.32)％,t=3.227,P=0.006],병반유조망상관단백Bcl-2/Bax상조(0.103±0.045、0.221±0.101,t=2.670,P=0.015).결론 결혈예괄응대병정4주당뇨병대서심기결혈/재관주손상구유보호효응,기통과상조조망상관기인Bcl-2/Bax,감소심기세포조망.
Objective To investigate the protective effects of ischemic preconditioning on myocardial ischemia/reperfusion injury in diabetic rats.Methods Twenty-eight healthy male rats were injected streptozotocin at dose of 45 mg/kg by tail and be fed with normal diet for 4 weeks,then rats were randomly divided into iscbemia/reperfusion (I/R) group and ischemic preconditioning (IP) group.ST segment of electrocardiograph changes and arrhythmias of all rats were recorded before ischemia and 0,15,30 minuets after ischemia and 0.5,2 h after reperfusion.TTC staining was performed to determine myocardial infarct size.TUNEL assay was used to assesse cardiomyocyte apoptosis.The expression of antiapoptotic gene (Bcl-2) and proapoptotic (Bax) was determined by immunohistochemistry.Results Compared with I/R group,ST segment elevation of patients in IP group decrease from (0.675 ±0.150) mV to (0.489 ±0.161) mV at 30 min after ischemia(P ＜0.05).Meanwhile the onset of ventricular premature contraction(VPC) in IP group was (18.21 ± 5.36) min,later than that of control group ((6.47 ± 4.28) min,t =5.241,P =0.000).The duration of VPC was (6.07 ± 4.33) min,shorter than that of I/R group ((16.71 ± 5.48) min,t =4.924,P ＜ 0.01)).The incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) of lP group remarkably decreased compared with I/R group (VT:57.14％ (8/14) vs.14.29％ (2/14),x2 =5.600,P =0.018 ; VF:50.00％ (7/ 14) vs.14.29％ (2/14),x2 =4.094,P=0.043).The myocardial infarct size in IP group was (12.50 ± 9.45) ％,smaller than that of I/R group ((37.50 ± 11.40)％,t =3.211,P =0.006).Cardiomyocyte apoptotic index (AI) was attenuated in IP group than that of I/R group((24.31 ± 3.12)％ vs.(19.01 ± 4.32)％,t =3.227,P =0.006),which was correlate with increased the ratio of Bcl-2/Bax((0.103 ±0.045) vs.(0.221 ±0.101),t =2.670,P =0.015).Conclusion IP treatment for diabetic rats shows a protect effect on myocardial I/R injury through attenuating myocardial apoptosis,and increasing the ratio of Bcl-2/Bax.
