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机构地区:[1]辽宁医学院附属第一医院麻醉科,锦州市121001
出 处:《临床麻醉学杂志》2011年第2期182-184,共3页Journal of Clinical Anesthesiology
摘 要:目的探讨核因子-κB(NF-κB)和细胞间粘附分子-1(ICAM-1)在七氟醚保护大鼠肝脏缺血-再灌注损伤机制中的作用。方法将40只SD成年雌性大鼠,随机均分为四组:假手术组(N组),缺血-再灌注组(IR组),七氟醚组(S组),七氟醚缺血-再灌注组(SIR组),每组10只。肝脏缺血1h、再灌注2h后取循环血和肝脏,N组、S组作为对照;IR组和SIR组阻断支配大鼠肝脏左叶和中叶的门静脉造成约70%肝脏缺血-再灌注模型,缺血1h、再灌注2h后取材。测定大鼠血清丙氨酸转氨酶(ALT)和天门冬氨酸转氨酶(AST)作为肝损害的标志被检测,光镜观察组织学病理改变,电镜下观察肝细胞的超微结构,采用免疫组织化学法检测肝组织NF-κB活性和ICAM-1水平。结果 SIR组肝ALT、AST酶升高受到显著抑制(P<0.05),电镜显示SIR组细胞损伤程度小于IR组,SIR组NF-κB和ICAM-1表达低于IR组(P<0.05)。结论七氟醚能抑制肝缺血-再灌注细胞的NF-κB和ICAM-1表达;NF-κB可能通过调控ICAM-1的表达在缺血-再灌注损伤中发挥作用。Objective To investigate the role of the nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in hepatic ischemia-reperfusion (IR) injury after scvoflurane preconditioning. Methods Forty female adult SD rats were randomly divided into 4 groups (n= 10): Sham operation group (N) ; Ischemia reperfusion group (IR) ; Sevoflurane group (S) ; Sevoflurane ischemia-reperfusion group (SIR). The animals were killed after hepatic ischemia reperfusion injury. Serum ALT and AST were detected as liver damage markers. The liver microscopy and uhrastructure were also obtained. The levels of NF-κB and ICAM-1 in the hepatic tissues were detected by immunohistochemistry. Results ALT and AST enzymes were significantly inhibited in SIR (P〈0. 05). The injury score of liver ultrastructure and the levels of NF-κB and ICAM-1 were lower in SIR than those in IR (P〈0.05). Conclusion Conclusion Sevoflurane inhibits hepatic expression of NF-κB and ICAM 1 after ischemia reperfusion injury. NF-κB might be a regulator of ICAM-1 in this process.
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