CAJ | 학술논문

目的观察大鼠肝脏缺血再灌注后TOLL样受体4(tolllike receptor4,Tlr-4)的表达,探讨丙泊酚肝脏保护作用及可能机制.方法 SD雄性大鼠56只,随机分为假手术(Sham)组、缺血/再灌注(I/R)组和丙泊酚(P)组.I/R组又进一步分为I/R2 h(I/R2)组、I/R6 h(I/R6)组和I/R24 h(I/R24)组;P组分为P2 h(P2)组、P6 h(P6)组和P24 h(P24)组.P组自缺血前30 min静脉输注丙泊酚1 mg·kg-1·min-1,Sham组及I/R组按0.1 mg·kg-1·min-1速率输注乳酸钠林格氏液,时间30 min.在相应的时间点处死动物,测定肿瘤坏死因子-α(TNF-α)、谷丙转氨酶(ALT)、谷草转氨酶(AST)水平及Tlr4的表达.结果 ①I/R组及P组再灌注后ALT、AST及TNF-α水平显著增高;但P组显著低于I/R组(P＜0.05).②Sham组仅有少量Tlr4蛋白表达;而I/R组及P组再灌注后表达量明显增加,但P组明显低于I/R组(P＜0.05).结论 TLRR4在肝脏I/R后被激活,在I/R损伤过程中发挥了重要作用.丙泊酚可部分降低再灌注后耶Tlr4的表达,减轻肝脏I/R损伤.
목적 관찰대서간장결혈재관주후TOLL양수체4(tolllike receptor4,Tlr-4)적표체,탐토병박분간장보호작용급가능궤제.방법 SD웅성대서56지,수궤분위가수술(Sham)조、결혈/재관주(I/R)조화병박분(P)조.I/R조우진일보분위I/R2 h(I/R2)조、I/R6 h(I/R6)조화I/R24 h(I/R24)조;P조분위P2 h(P2)조、P6 h(P6)조화P24 h(P24)조.P조자결혈전30 min정맥수주병박분1 mg·kg-1·min-1,Sham조급I/R조안0.1 mg·kg-1·min-1속솔수주유산납림격씨액,시간30 min.재상응적시간점처사동물,측정종류배사인자-α(TNF-α)、곡병전안매(ALT)、곡초전안매(AST)수평급Tlr4적표체.결과 ①I/R조급P조재관주후ALT、AST급TNF-α수평현저증고;단P조현저저우I/R조(P＜0.05).②Sham조부유소량Tlr4단백표체;이I/R조급P조재관주후표체량명현증가,단P조명현저우I/R조(P＜0.05).결론 TLRR4재간장I/R후피격활,재I/R손상과정중발휘료중요작용.병박분가부분강저재관주후야Tlr4적표체,감경간장I/R손상.
Objective To observe the changes in TLR4 expression during hepatic ischemia/reperfusion (I/R) and the effects of propofol on the expression of TLR4 induced by I/R injury in rats.Methods Fifty six male SD rats were randomly divided into min before isehemia in P groups,and the same volume of sodium lactate Ringer's solution was infused in sham group and I/R groups.Plasma ALT,AST,TNF-α levels were measured,and the expression of Tlr4 was detected 2,6,24 h after reperfusion.Results The levels of plasma ALT,AST and TNF-α were lower,and Tlr4 expression was weaker in P groups than those in I/R groups (P＜0.05).Conclusion Propofol decreases hepatic ischemia/reperfusion (I/R)-induced Tlr4 expression and exerts property of liver protection.