硫辛酸灌胃对大鼠肾缺血再灌注后肝损伤的防治作用及机制探讨

发布时间：2018-05-16 13:35

本文选题：硫辛酸 + 缺血再灌注损伤　；参考：《山东医药》2017年47期

【摘要】：目的观察硫辛酸(LA)灌胃对大鼠肾缺血再灌注(RIR)后肝损伤的防治作用,并探讨其机制。方法30只SD大鼠随机分为3组各10只,对照组及模型组常规饲养,实验组灌胃给予250 mg/(kg·24 h)的LA,连续饲养4周。实验组及模型组制备RIR模型,对照组除不夹闭双侧肾动、静脉外,其余操作均与实验组及模型组相同。检测各组血浆肌酐(Scr)、尿素氮(BUN)、谷草转氨酶(ALT)、谷丙转氨酶(AST)、一氧化氮(NO)和肝组织Ca2+、黄嘌呤氧化酶(XOD)、活性氧(ROS)、丙二醛(MDA)、髓过氧化物酶(MPO),比较肝细胞线粒体Ca2+及Na+-K+-依赖ATP提供能量运转的离子泵(ATPase)、Ca2+-Mg2+-ATPase、谷胱甘肽过氧化物酶(GSH-Px)活性,观察肝组织ICAM-1、Caspase-3、Hsp70蛋白表达情况。结果与对照组比较,模型组血浆Scr、BUN、ALT、AST、NO升高,肝组织Ca2+、XOD、ROS、MDA、MPO升高,肝线粒体Ca2+升高,Na+-K+-ATPase、Ca2+-Mg2+-ATPase、GSH-Px活性降低;ICAM-1蛋白表达增强,肝组织Caspase-3、Hsp70阳性率升高。与模型组比较,实验组血浆Scr、BUN、ALT、AST降低,肝组织Ca2+、XOD、ROS、MDA降低,肝线粒体Ca2+降低,Na+-K+-ATPase、Ca2+-Mg2+-ATPase、GSH-Px活性升高,血浆NO升高,肝组织MPO降低,ICAM-1表达减弱,Caspase-3阳性细胞数减少,Hsp70阳性细胞数增多。结论 LA对RIR后肝损伤有防治作用,其机制可能通过抗氧化、保护线粒体、抑制炎症因子、抗凋亡等途径来实现。
[Abstract]:Objective to observe the prevention and treatment of hepatic injury after renal ischemia reperfusion (RIR) in rats by intragastric administration of lipoxylic acid (LAA), and to explore its mechanism. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups (10 rats in each group). The control group and the model group were fed with LA250 mg/(kg for 24 h by gavage for 4 weeks. The RIR model was made in the experimental group and the model group. The control group had the same operation as the experimental group and the model group except for the bilateral renal artery and vein. The levels of plasma creatinine, bun, glutamic oxalacetic transaminase (alt), alanine aminotransferase (alt), nitric oxide (no) and liver Ca2 were detected. Xanthine oxidase (XODO), reactive oxygen species (Ros), malondialdehyde (malondialdehyde) (MDA) and myeloperoxidase (MPO) were used to compare the activities of mitochondrial Ca2 and Na-K-dependent ATP (Ca 2-mg 2-AT Paseate), glutathione peroxidase (glutathione peroxidase) GSH-Px, and to observe the expression of ICAM-1Caspase-3 Hsp70 protein in liver tissue. Results compared with the control group, the level of plasma Scr-BUNTN ASTN in the model group was higher than that in the control group, the Ca2 XODS-ROSDA MPO in the liver tissue was increased, and the activity of Ca2 in the mitochondria of the liver was increased. The activity of GSH-Px in the liver mitochondria was decreased and the expression of ICAM-1 protein was increased. The positive rate of Caspase-3 Hsp70 in the liver tissue was increased. Compared with the model group, the plasma Scr-BUNT AST decreased, the Ca2 XODROSMDA decreased, the hepatic mitochondrial Ca2 decreased the activity of Na -K -AT Paseate Ca 2 -mg 2 -ATP Paseum GSH-Px, the plasma no increased, the MPO decreased the expression of ICAM-1 and the number of Caspase-3 positive cells decreased and the number of Hsp70 positive cells increased in the experimental group. Conclusion LA has protective effect on liver injury after RIR, and its mechanism may be through anti-oxidation, protecting mitochondria, inhibiting inflammatory factors, anti-apoptosis and so on.
【作者单位】：华北理工大学;
【基金】：国家自然科学基金资助项目(81600316) 大学生创新课题(X2017179)
【分类号】：R692

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