摘要
目的探讨PGE1对脂肪肝缺血再灌注损伤的保护作用及可能的机制。方法 42只雄性Wistar大鼠建立脂肪肝模型,随机分成实验组和对照组。对大鼠门静脉进行插管,实验组给予5μg/mL PGE1,以0.1mL/kg·min速度持续给药15 min,对照组给予等量生理盐水,然后随即行Pringle’法阻断肝门15 min。分别于再灌注1、6及24 h,测定动脉血清中生化酶水平(ALT、AST),Western Blot的方法检测p-NF-кB p65的表达,免疫组织化学染色检测ICAM-1的表达。结果脂肪肝缺血再灌注损伤早期ALT、AST、p-NF-кB p65及ICAM-1表达均逐渐升高,6 h达高峰,随后逐渐降低。PGE1干预后可以明显减少脂肪肝缺血再灌注损伤所引起的ALT、AST、p-NF-кB p65及ICAM-1的表达。结论术前、术中持续输注PGE1对脂肪肝缺血再灌注损伤具有明显的保护作用,其作用通过抑制NF-кB的核转位,继而下调ICAM-1表达实现。
【Objective】To explore the protection of PGE1 on ischemic reperfusion injury of fat liver and the potential mechanism.【Methods】Rat models of fatty liver were established in the beginning. 42 Male Wistar rats were randomly divided into the experimental group and control group. Polyethylene catheter was inserted into the branch of superior mesenteric vein, rats were given 5μg/mL PGE1 by 0.1 mL/kg·min in the experimental group, rats were given the same saline in the control group. After15 min, the hepatic hilum was blocked for 15 minutes by Pringle's method. The level of ALT and AST were measured by whole automatic biochemistry analyzer. The expression of pNF-кB p65 was detected by western blot. The expression of ICAM-1 was detected by immunohistochemistry.【Results】In the early stage of ischemic reperfusion injury of fat liver, the level of ALT、AST、p-NF-кB p65 and ICAM-1 were increased gradually, the peak value occurred at 6 hours after ischemic reperfusion injury, whereafter the level of them cut down gradually. PGE1 could decrease the expression of ALT、AST、p-NF-кB p65 and ICAM-1 induced by ischemic reperfusion injury of fat liver.【Conclusions】The continuous infusion of PGE1 before and during operation played an obvious protection role on ischemic reperfusion injury of fat liver by inhibiting nuclear translocation of NF-кB and decreasing the expression of ICAM-1.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2014年第12期7-11,共5页
China Journal of Modern Medicine
基金
辽宁省自然科学基金资助项目(No:2013021068)