异丙酚预处理对大鼠肝脏缺血再灌注损伤时自噬的影响

发布时间：2018-04-21 00:09

本文选题：异丙酚 + 肝脏　；参考：《安徽医科大学学报》2017年12期

【摘要】：目的评价异丙酚预处理对大鼠肝脏缺血再灌注损伤时自噬的影响。方法健康成年雄性SD大鼠50只,体重240~280 g,采用随机数字表法,将SD大鼠随机分为5组(n=10):假手术组(S组);异丙酚单独给药组(P组):经股静脉以12 mg/(kg·h)持续泵注1%异丙酚45 min;肝脏缺血再灌注组(HIR组):血管夹钳夹支配肝左叶、中叶的肝蒂,造成70%肝脏缺血,1 h后放开血管夹恢复血供造成缺血再灌注损伤;异丙酚预处理组(PHIR组):于缺血前30 min经股静脉泵注异丙酚12 mg/(kg·h)30 min至缺血15 min;脂肪乳预处理组(IHIR组):于缺血前30 min经股静脉泵注脂肪乳1.2 ml/(kg·h)30 min至缺血15 min。于再灌注6 h时,处死大鼠取腹主动脉血测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性,取肝左叶肝脏采用Western blot法检测自噬标志物LC3-Ⅱ、LC3-Ⅰ及Beclin-1的表达水平。结果电镜显示,S组细胞结构正常,未见自噬体,而HIR组可见大量自噬体及自噬溶酶体,PHIR组细胞结构基本正常,少见自噬体;与S组相比,HIR组肝细胞电镜下见大量富含血清ALT和AST活性增高,肝组织LC3-Ⅱ/LC3-Ⅰ比值及Beclin-1表达上调(P0.05),P组各项指标差异无统计学意义;与HIR组相比,PHIR组血清ALT和AST活性显著降低,肝组织LC3-Ⅱ/LC3-Ⅰ比值及Beclin-1表达显著下调(P0.05),而IHIR组各项指标差异无统计学意义。结论异丙酚预处理减轻大鼠肝脏缺血再灌注损伤机制可能与抑制肝细胞自噬激活有关。
[Abstract]:Objective to evaluate the effect of propofol preconditioning on autophagy in rat liver ischemia-reperfusion injury. Methods 50 healthy adult male SD rats, weighing 240~280 g, were randomly divided into 5 groups (n=10): the sham operation group (group S), the individual propofol group (group P): 12 mg/ (kg h) continuous infusion of 1% propofol through the femoral vein. 45 min; liver ischemia reperfusion group (group HIR): vascular clamp clamp dominates the left lobe of the liver, the liver pedicle of the middle lobe, causes 70% liver ischemia, and after 1 h, release blood supply to restore the ischemia reperfusion injury; the propofol preconditioning group (group PHIR): 12 mg/ (kg. H) 30 min to 15 min; preconditioning of fat emulsion at 30 min before ischemia Group (group IHIR): the activity of serum alanine aminotransferase (ALT) and glutarine aminotransferase (AST) in the abdominal aorta of rats was killed at 30 min before ischemia by injection of fat milk 1.2 ml/ (kg. H) 30 min to 15 min. at 6 h, and the liver left lobe liver was taken by Western blot method to detect autophagic markers The results showed that the cell structure of S group was normal and no autophagosome was found, while a large number of autophagosomes and autophagosomes were found in group HIR. The cell structure of group PHIR was basically normal, and the autophagosome was rare. Compared with the S group, a large number of serum ALT and AST activities were high in the HIR group, and the ratio of LC3- II /LC3- I and the expression of Beclin-1 in the liver tissue were up. (P0.05), there was no significant difference in the indexes of group P. Compared with group HIR, the activity of ALT and AST in the serum of PHIR group decreased significantly, the ratio of LC3- II /LC3- I and Beclin-1 expression in liver tissue decreased significantly (P0.05), but there was no significant difference in the indexes of IHIR group. Conclusion the mechanism of propofol pretreatment alleviated the mechanism of liver ischemia reperfusion injury in rats. Inhibition of the activation of autophagy in the liver cells.

【作者单位】：安徽医科大学第一附属医院麻醉科;安徽医科大学生物药物研究所;
【基金】：教育部高等学校博士学科点专项科研基金(编号:20133420110009)
【分类号】：R614

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