中国医药指南
中國醫藥指南
중국의약지남
CHINA MEDICINE GUIDE
2012年
36期
14-15
,共2页
七氟烷后处理%缺血再灌注损伤%细胞凋亡%p53
七氟烷後處理%缺血再灌註損傷%細胞凋亡%p53
칠불완후처리%결혈재관주손상%세포조망%p53
Sevoflurance postconditioning%Ischemic-reperfusion injury%Apoptosis%p53
目的探讨七氟烷后处理对大鼠在体心肌缺血再灌注时细胞凋亡的影响.方法将40只雄性 SD 大鼠随机分为5组(n=8):假手术组(S 组);缺血再灌注组(IR 组);1%、2%、3%七氟烷后处理组(SP1、SP2、SP3组),建立心肌缺血再灌注模型,再灌注结束时测定血清 LDH 浓度、心肌 p53蛋白表达水平和细胞凋亡.结果与 S 组比较,各组血清 LDH 浓度、心肌 p53蛋白表达和细胞凋亡升高(P <0.05);与 IR 组比较,各 SP 组血清 LDH 浓度、心肌 p53蛋白表达和细胞凋亡降低(P <0.05);与 SP2组比较,SP1组和 SP3组血清 LDH 浓度、心肌 p53蛋白表达和细胞凋亡升高(P <0.05).结论七氟烷后处理可通过下调 p53蛋白表达抑制细胞凋亡,从而减轻大鼠心肌缺血再灌注损伤,2%七氟烷后处理的效果更显著.
目的探討七氟烷後處理對大鼠在體心肌缺血再灌註時細胞凋亡的影響.方法將40隻雄性 SD 大鼠隨機分為5組(n=8):假手術組(S 組);缺血再灌註組(IR 組);1%、2%、3%七氟烷後處理組(SP1、SP2、SP3組),建立心肌缺血再灌註模型,再灌註結束時測定血清 LDH 濃度、心肌 p53蛋白錶達水平和細胞凋亡.結果與 S 組比較,各組血清 LDH 濃度、心肌 p53蛋白錶達和細胞凋亡升高(P <0.05);與 IR 組比較,各 SP 組血清 LDH 濃度、心肌 p53蛋白錶達和細胞凋亡降低(P <0.05);與 SP2組比較,SP1組和 SP3組血清 LDH 濃度、心肌 p53蛋白錶達和細胞凋亡升高(P <0.05).結論七氟烷後處理可通過下調 p53蛋白錶達抑製細胞凋亡,從而減輕大鼠心肌缺血再灌註損傷,2%七氟烷後處理的效果更顯著.
목적탐토칠불완후처리대대서재체심기결혈재관주시세포조망적영향.방법장40지웅성 SD 대서수궤분위5조(n=8):가수술조(S 조);결혈재관주조(IR 조);1%、2%、3%칠불완후처리조(SP1、SP2、SP3조),건립심기결혈재관주모형,재관주결속시측정혈청 LDH 농도、심기 p53단백표체수평화세포조망.결과여 S 조비교,각조혈청 LDH 농도、심기 p53단백표체화세포조망승고(P <0.05);여 IR 조비교,각 SP 조혈청 LDH 농도、심기 p53단백표체화세포조망강저(P <0.05);여 SP2조비교,SP1조화 SP3조혈청 LDH 농도、심기 p53단백표체화세포조망승고(P <0.05).결론칠불완후처리가통과하조 p53단백표체억제세포조망,종이감경대서심기결혈재관주손상,2%칠불완후처리적효과경현저.
Objective To investigate the effects of sevoflurane postconditioning on cardiomyocyte apoptosis following myocardial ischemia-reperfusion in vivo rat heart. Methods Forty male SD rats were randomly divided into 5 groups(n=8 each):sham operation group(group S); ischemia-reperfusion(group IR);1%, 2%, 3% sevoflurane postconditioning group(group SP1, SP2, SP3). Establishing the model of myocardial ischemia reperfusion and measuring serum LDH concentrations、myocardial p53 expression and apoptosis at the end of the reperfusion. Results Serum LDH concentrations, myocardial p53 expression and apoptosis were higher in the other groups than in S group(P<0.05); Compared with IR group, SP group showed reduced serum LDH concentrateons, the myocardial p53 expression and apoptosis (P<0.05); Serum LDH concentrationns, myocardial p53 expression and apoptosis were higher in SP1 and SP3 groups than in SP2 group (P<0.05). Conclusion Sevoflurane postconditioning can possible through downregulation of p53 expression to inhibit apoptosis, thereby relieving myocardial ischemia-reperfusion injury in rats, and 2% sevoflurane postconditioning has a more significant effect.
