西安交通大学学报(医学版)
西安交通大學學報(醫學版)
서안교통대학학보(의학판)
JOURNAL OF XI'AN JIAOTONG UNIVERSITY(MEDICAL SCIENCES)
2014年
3期
357-360
,共4页
赵文晖%陈军%景桂霞%刘健%党晓东
趙文暉%陳軍%景桂霞%劉健%黨曉東
조문휘%진군%경계하%류건%당효동
异丙酚%心肌再灌注损伤%Toll样受体4%肿瘤坏死因子-α%核转录因子
異丙酚%心肌再灌註損傷%Toll樣受體4%腫瘤壞死因子-α%覈轉錄因子
이병분%심기재관주손상%Toll양수체4%종류배사인자-α%핵전록인자
propofol%mycardial reperfusion injury%Toll-like receptor 4%tumor necrosis factor-α%NF-kappa B
目的:探讨异丙酚对大鼠缺血再灌注心肌 Toll 样受体(TLR-4)、肿瘤坏死因子-α(TNF-α)和核转录因子(NF-κb)的影响。方法健康雄性 SD大鼠30只,体质量250~320 g,随机分为3组,每组10只。对照组(A组)左冠状动脉前降支穿线;缺血再灌注组(B组)左冠状动脉前降支穿线结扎30 min后,再灌注120 min;异丙酚组(C组)缺血前10 min经股静脉持续静脉注射异丙酚5 mg/(kg·h),输注至再灌注结束。3组再灌注120 min后,通过透射电镜观察心肌细胞超微结构的改变,并测定心肌TLR-4、TNF-α及 NF-κb 蛋白的表达。结果透射电镜下观察超微结构显示,B组、C组较 A组明显加重了心肌组织结构和线粒体的损害,C 组损伤较轻。与 A 组比较,B、C 组心肌 TLR-4、TNF-α及 NF-κb蛋白表达上调,C组较B组心肌TLR-4、TNF-α及 NF-κb蛋白表达下调。结论静脉注射异丙酚可保护心肌受损,并抑制大鼠缺血再灌注心肌TLR-4、TNF-α及 NF-κb的表达。
目的:探討異丙酚對大鼠缺血再灌註心肌 Toll 樣受體(TLR-4)、腫瘤壞死因子-α(TNF-α)和覈轉錄因子(NF-κb)的影響。方法健康雄性 SD大鼠30隻,體質量250~320 g,隨機分為3組,每組10隻。對照組(A組)左冠狀動脈前降支穿線;缺血再灌註組(B組)左冠狀動脈前降支穿線結扎30 min後,再灌註120 min;異丙酚組(C組)缺血前10 min經股靜脈持續靜脈註射異丙酚5 mg/(kg·h),輸註至再灌註結束。3組再灌註120 min後,通過透射電鏡觀察心肌細胞超微結構的改變,併測定心肌TLR-4、TNF-α及 NF-κb 蛋白的錶達。結果透射電鏡下觀察超微結構顯示,B組、C組較 A組明顯加重瞭心肌組織結構和線粒體的損害,C 組損傷較輕。與 A 組比較,B、C 組心肌 TLR-4、TNF-α及 NF-κb蛋白錶達上調,C組較B組心肌TLR-4、TNF-α及 NF-κb蛋白錶達下調。結論靜脈註射異丙酚可保護心肌受損,併抑製大鼠缺血再灌註心肌TLR-4、TNF-α及 NF-κb的錶達。
목적:탐토이병분대대서결혈재관주심기 Toll 양수체(TLR-4)、종류배사인자-α(TNF-α)화핵전록인자(NF-κb)적영향。방법건강웅성 SD대서30지,체질량250~320 g,수궤분위3조,매조10지。대조조(A조)좌관상동맥전강지천선;결혈재관주조(B조)좌관상동맥전강지천선결찰30 min후,재관주120 min;이병분조(C조)결혈전10 min경고정맥지속정맥주사이병분5 mg/(kg·h),수주지재관주결속。3조재관주120 min후,통과투사전경관찰심기세포초미결구적개변,병측정심기TLR-4、TNF-α급 NF-κb 단백적표체。결과투사전경하관찰초미결구현시,B조、C조교 A조명현가중료심기조직결구화선립체적손해,C 조손상교경。여 A 조비교,B、C 조심기 TLR-4、TNF-α급 NF-κb단백표체상조,C조교B조심기TLR-4、TNF-α급 NF-κb단백표체하조。결론정맥주사이병분가보호심기수손,병억제대서결혈재관주심기TLR-4、TNF-α급 NF-κb적표체。
Objective To investigate the effects of propofol on the changes in myocardial Toll-like receptor 4 (TLR-4)and TNF-αand NF-κb protein expressions in ischemia-reperfusion injury (I/R).Methods Thirty healthy male SD rats weighing 250-320 g were randomly divided into 3 groups (n=10 for each):Group A,sham operation;Group B,I/R;and Group C,propofol + I/R.In Groups B and C myocardial I/R was induced by occlusion of the left anterior descending artery (LAD)for 30 min,followed by 120 min reperfusion.In Group C propofol was given intravenously 1 0 min before myocardial ischemia,followed by continuous infusion of propofol at 5 mg/(kg·h)until the end of 120 min reperfusion.In Groups A and B normal saline instead of propofol was given. The myocardial tissues were taken at the end of 120 min;ultrastructural changes of myocardial cells were observed under X-ray electron microscope and the expressions of TLR-4 mRNA as well as TNF-αand NF-κb protein were determined.Results Ultrastructural observation under electron microscope showed significantly worsened damage in myocardial tissue structure and mitochondria in Groups B and C compared with Group A.The myocardial expressions of TLR-4 and TNF-αand NF-κb protein were significantly higher in Groups B and C than in control Group A.The myocardial expressions of TLR-4 and TNF-αand NF-κb protein were down-regulated in Group C compared with Group B.Conclusion Intravenous injection of propofol can protect against myocardial damage.Propofol can suppress the increase in myocardial TLR-4 and TNF-αand NF-κb protein expressions induced by I/R.