中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
6期
665-667
,共3页
李冬梅%金笛%王琦%邓希锦%隋海静%林长赋%丁文刚%李文志
李鼕梅%金笛%王琦%鄧希錦%隋海靜%林長賦%丁文剛%李文誌
리동매%금적%왕기%산희금%수해정%림장부%정문강%리문지
二异丙酚%糖尿病,2型%心肌再灌注损伤%细胞凋亡
二異丙酚%糖尿病,2型%心肌再灌註損傷%細胞凋亡
이이병분%당뇨병,2형%심기재관주손상%세포조망
Propofol%Diabetes mellitus,type 2%Myocardial reperfusion injury%Apoptosis
目的 探讨异丙酚对2型糖尿病大鼠心肌缺血再灌注时细胞凋亡的影响.方法 成年雄性Wistar大鼠,体重160~ 180 g,腹腔注射链脲佐菌素30 mg/kg,1次/d,连续2d,制备2型糖尿病模型.取2型糖尿病模型制备成功的大鼠24只,采用随机数字表法,将其分为3组(n=8):假手术组(S组)、心肌缺血再灌注组(I/R组)和异丙酚组(P组).采用结扎左冠状动脉前降支30 min,再灌注2h的方法制备心肌缺血再灌注损伤模型.P组于缺血前10 min开始静脉输注异丙酚6 mg·kg-1·h-1至再灌注2h.再灌注2h时处死大鼠,取缺血区心肌组织,光镜下观察病理学结果,采用TUNEL法检测心肌细胞凋亡情况,计算凋亡指数(AI);采用免疫组化法测定Bax和Bcl-2的表达水平;采用Westernblot法检测caspase-3表达水平.结果 与S组比较,I/R组和P组心肌组织Bcl-2、Bax和caspase-3的表达上调,AI升高(P<0.05),心肌发生病理学损伤;与I/R组比较,P组心肌组织Bax和caspase-3表达下调,Bcl-2表达上调,AI降低(P<0.05),心肌病理学损伤减轻.结论 异丙酚减轻糖尿病大鼠心肌缺血再灌注损伤的机制与上调Bcl-2表达,下调Bax和caspase-3的表达,抑制细胞凋亡有关.
目的 探討異丙酚對2型糖尿病大鼠心肌缺血再灌註時細胞凋亡的影響.方法 成年雄性Wistar大鼠,體重160~ 180 g,腹腔註射鏈脲佐菌素30 mg/kg,1次/d,連續2d,製備2型糖尿病模型.取2型糖尿病模型製備成功的大鼠24隻,採用隨機數字錶法,將其分為3組(n=8):假手術組(S組)、心肌缺血再灌註組(I/R組)和異丙酚組(P組).採用結扎左冠狀動脈前降支30 min,再灌註2h的方法製備心肌缺血再灌註損傷模型.P組于缺血前10 min開始靜脈輸註異丙酚6 mg·kg-1·h-1至再灌註2h.再灌註2h時處死大鼠,取缺血區心肌組織,光鏡下觀察病理學結果,採用TUNEL法檢測心肌細胞凋亡情況,計算凋亡指數(AI);採用免疫組化法測定Bax和Bcl-2的錶達水平;採用Westernblot法檢測caspase-3錶達水平.結果 與S組比較,I/R組和P組心肌組織Bcl-2、Bax和caspase-3的錶達上調,AI升高(P<0.05),心肌髮生病理學損傷;與I/R組比較,P組心肌組織Bax和caspase-3錶達下調,Bcl-2錶達上調,AI降低(P<0.05),心肌病理學損傷減輕.結論 異丙酚減輕糖尿病大鼠心肌缺血再灌註損傷的機製與上調Bcl-2錶達,下調Bax和caspase-3的錶達,抑製細胞凋亡有關.
목적 탐토이병분대2형당뇨병대서심기결혈재관주시세포조망적영향.방법 성년웅성Wistar대서,체중160~ 180 g,복강주사련뇨좌균소30 mg/kg,1차/d,련속2d,제비2형당뇨병모형.취2형당뇨병모형제비성공적대서24지,채용수궤수자표법,장기분위3조(n=8):가수술조(S조)、심기결혈재관주조(I/R조)화이병분조(P조).채용결찰좌관상동맥전강지30 min,재관주2h적방법제비심기결혈재관주손상모형.P조우결혈전10 min개시정맥수주이병분6 mg·kg-1·h-1지재관주2h.재관주2h시처사대서,취결혈구심기조직,광경하관찰병이학결과,채용TUNEL법검측심기세포조망정황,계산조망지수(AI);채용면역조화법측정Bax화Bcl-2적표체수평;채용Westernblot법검측caspase-3표체수평.결과 여S조비교,I/R조화P조심기조직Bcl-2、Bax화caspase-3적표체상조,AI승고(P<0.05),심기발생병이학손상;여I/R조비교,P조심기조직Bax화caspase-3표체하조,Bcl-2표체상조,AI강저(P<0.05),심기병이학손상감경.결론 이병분감경당뇨병대서심기결혈재관주손상적궤제여상조Bcl-2표체,하조Bax화caspase-3적표체,억제세포조망유관.
Objective To investigate the effects of propofol on cell apoptosis during myocardial ischemiareperfusion (I/R) in rats with type 2 diabetes mellitus (DM).Methods Adult male Wistar rats,weighing 160-180 g,were used in this study.Type 2 DM was induced by intraperitoneal streptozotocin (STZ) 30 mg/kg once a day for 2 consecutive days.Twenty-four animals with type 2 DM were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),I/R group and propofol group (group P).Myocardial I/R was produced by occlusion of the anterior descending branch of left coronary artery for 30 min followed by 2 h reperfusion.Propofol was infused intravenously at 6 mg· kg-1 · h-1 starting from 10 min before ischemia until 2 h of reperfusion in group P.The animals were sacrificed after 2 h of reperfusion and myocardial specimens in the ischemic region were obtained for microscopic examination and for determination of cell apoptosis and expression of Bax,Bcl-2 and caspase-3.The apoptosis index (AI) was calculated.Results Compared with group S,the expression of Bcl-2,Bax and caspase-3 was significantly up-regulated,and AI was increased,and microscopic examination showed that pathological changes of myocardium were found in I/R and P groups.Compared with group I/R,the expression of Bax and caspase-3 was significantly down-regulated,Bcl-2 expression was up-regulated,AI was decreased,and the pathologic changes were attenuated in group P.Conclusion The mechanism by which propofol attenuates myocardial I/R injury is related to up-regulation of Bcl-2 expression,down-regulation of Bax and caspase-3 expression and inhibition of cell apoptosis in rats with type 2 DM.