中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
6期
746-749
,共4页
磷酸肌酸%糖尿病,实验性%心肌再灌注损伤%细胞凋亡
燐痠肌痠%糖尿病,實驗性%心肌再灌註損傷%細胞凋亡
린산기산%당뇨병,실험성%심기재관주손상%세포조망
Phosphocreatine%Diabetes mellitus,experimental%Myocardial repeffusion injury%Apoptosis
目的 探讨磷酸肌酸对糖尿病大鼠心肌缺血再灌注时细胞凋亡的影响.方法 雄性SD大鼠,体重150～170 g,采用高脂饲养联合腹腔注射链脲佐菌素的方法制备糖尿病模型,造模成功的27只大鼠饲养2周后,采用随机数字表法,将其随机分为3组(n=9):假手术组(S组)、缺血再灌注组(I/R组)和磷酸肌酸组(PP组).I/R组和PP组采用结扎左冠状动脉前降支30 min再灌注2 h的方法制备心肌缺血再灌注模型,PP组于缺血前30 min腹腔注射磷酸肌酸1g/kg,I/R组给予等容量生理盐水.再灌注2 h时采集静脉血样,测定血浆肌钙蛋白T(cTnT)的浓度,然后处死大鼠,取心肌组织,采用免疫组化法测定Bcl-2、Bax和Caspase-3表达的水平,并计算Bcl-2与Bax表达的比值(Bcl-2/Bax 比),采用TUNEL染色法检测细胞凋亡情况,计算凋亡指数(AI);电镜下观察心肌细胞超微结构.结果 与S组比较,I/R组血浆cTnT浓度升高,心肌组织Bcl-2、Bax和Caspase-3表达上调,Bcl-2/Bax比降低,AI升高(P＜0.05或0.01);与I/R组比较,PP组血浆cTnT浓度降低,心肌组织Bcl-2表达上调,Bax和Caspase-3表达下调,Bcl-2/Bax比升高,AI降低(P＜0.01).PP组心肌病理学损伤程度轻于I/R组.结论 磷酸肌酸可抑制细胞凋亡,从而减轻糖尿病大鼠心肌缺血再灌注损伤,其机制与上调Bcl-2表达、下调Bax和Caspase-3的表达有关.
目的 探討燐痠肌痠對糖尿病大鼠心肌缺血再灌註時細胞凋亡的影響.方法 雄性SD大鼠,體重150～170 g,採用高脂飼養聯閤腹腔註射鏈脲佐菌素的方法製備糖尿病模型,造模成功的27隻大鼠飼養2週後,採用隨機數字錶法,將其隨機分為3組(n=9):假手術組(S組)、缺血再灌註組(I/R組)和燐痠肌痠組(PP組).I/R組和PP組採用結扎左冠狀動脈前降支30 min再灌註2 h的方法製備心肌缺血再灌註模型,PP組于缺血前30 min腹腔註射燐痠肌痠1g/kg,I/R組給予等容量生理鹽水.再灌註2 h時採集靜脈血樣,測定血漿肌鈣蛋白T(cTnT)的濃度,然後處死大鼠,取心肌組織,採用免疫組化法測定Bcl-2、Bax和Caspase-3錶達的水平,併計算Bcl-2與Bax錶達的比值(Bcl-2/Bax 比),採用TUNEL染色法檢測細胞凋亡情況,計算凋亡指數(AI);電鏡下觀察心肌細胞超微結構.結果 與S組比較,I/R組血漿cTnT濃度升高,心肌組織Bcl-2、Bax和Caspase-3錶達上調,Bcl-2/Bax比降低,AI升高(P＜0.05或0.01);與I/R組比較,PP組血漿cTnT濃度降低,心肌組織Bcl-2錶達上調,Bax和Caspase-3錶達下調,Bcl-2/Bax比升高,AI降低(P＜0.01).PP組心肌病理學損傷程度輕于I/R組.結論 燐痠肌痠可抑製細胞凋亡,從而減輕糖尿病大鼠心肌缺血再灌註損傷,其機製與上調Bcl-2錶達、下調Bax和Caspase-3的錶達有關.
목적 탐토린산기산대당뇨병대서심기결혈재관주시세포조망적영향.방법 웅성SD대서,체중150～170 g,채용고지사양연합복강주사련뇨좌균소적방법제비당뇨병모형,조모성공적27지대서사양2주후,채용수궤수자표법,장기수궤분위3조(n=9):가수술조(S조)、결혈재관주조(I/R조)화린산기산조(PP조).I/R조화PP조채용결찰좌관상동맥전강지30 min재관주2 h적방법제비심기결혈재관주모형,PP조우결혈전30 min복강주사린산기산1g/kg,I/R조급여등용량생리염수.재관주2 h시채집정맥혈양,측정혈장기개단백T(cTnT)적농도,연후처사대서,취심기조직,채용면역조화법측정Bcl-2、Bax화Caspase-3표체적수평,병계산Bcl-2여Bax표체적비치(Bcl-2/Bax 비),채용TUNEL염색법검측세포조망정황,계산조망지수(AI);전경하관찰심기세포초미결구.결과 여S조비교,I/R조혈장cTnT농도승고,심기조직Bcl-2、Bax화Caspase-3표체상조,Bcl-2/Bax비강저,AI승고(P＜0.05혹0.01);여I/R조비교,PP조혈장cTnT농도강저,심기조직Bcl-2표체상조,Bax화Caspase-3표체하조,Bcl-2/Bax비승고,AI강저(P＜0.01).PP조심기병이학손상정도경우I/R조.결론 린산기산가억제세포조망,종이감경당뇨병대서심기결혈재관주손상,기궤제여상조Bcl-2표체、하조Bax화Caspase-3적표체유관.
Objective To investigate the effects of phosphocreatine on apoptosis following myocardial ischemia-reperfusion (I/R) in diabetic rats. Methods Male SD rats weighing 150-170 g were used in this study.Diabetes mellitus was induced by high fat diet and intraperitoneal streptozotocin. Twenty-seven rats in which diabetes mellitus was successfully induced were randomly divided into 3 groups ( n = 9 each): sham operation group (group S);myocardial I/R group(group I/R )and phosphocreatine group (group PP). Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 2 h reperfusion in I/R and PP groups. In group PP phosphocreatine 1 g/kg was given intraperitoneally 30 min before myocardial I/R. Blood samples were collected at the end of 2 h reperfusion for determination of plasma concentration of calcium troponin T (cTnT). The animals were then sacrificed and iscbemic myocardial specimens were isolated. The expression of Bcl-2, Bax and Caspase-3 in isehemic myocarcdium was determined and Bcl-2/Bax ratio was calculated. Myocardial apoptosis was detected by TUNEL and apoptotic index was calculated. The ultrastructure of cardiomyocytes was examined with electron microscope. Results Myocardial I/R significantly increased plasma cTnT concentration and Bcl-2, Bax and Caspase-3 expression in myocardium and apoptosis index and decreased Bcl-2/Bax ratio. Phosphocreatine significantly attenuated I/R-induced above-mentioned changes and myocardial damage. Conclusion Phosphocreatine can reduce myocardial I/R injury in diabetic mellitus rats by reducing myocardial apoptosis through up-regulation of Bcl-2 expression and down-regulation of Bax and Caspase-3 expression.
