黄芪多糖对大鼠肝脏缺血再灌注损伤的影响

Effect of Astragalus Polysaccharide on Hepatic Ischemia Reperfusion Injury in Rats

目的:观察黄芪多糖(Astragalus Polysaccharide,APS)对大鼠肝脏缺血再灌注损伤的影响及可能的保护机制。方法:30只SD雄性大鼠随机分为3组,每组10只:假手术组、模型组、黄芪多糖组。造模前,黄芪多糖组给予黄芪多糖30 mg·kg-1尾静脉注射,1次/天;假手术组和模型组给予相同剂量的生理盐水,连续7 d。建立70%的大鼠肝脏缺血再灌注损伤模型,缺血1 h后再灌注4 h。取腹主动脉血测谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)含量。取大鼠肝脏,检测肝脏组织匀浆中SOD(超氧化物歧化酶)活性和MDA(丙二醛)含量;ELISA法检测炎症因子IL-1β(白介素-1β)、TNF-α(肿瘤坏死因子-α)、IL-10(白介素-10)水平;免疫组化法检测肝脏组织HO-1(血红素加氧酶-1)的表达水平,光镜下观察肝脏病理学变化。结果:与假手术组相比,模型组和黄芪多糖组血清ALT、AST、LDH含量显著升高(均P<0.01);黄芪多糖组三者水平显著低于模型组(均P<0.01)。与假手术组相比,模型组和黄芪多糖组肝组织SOD活性显著下降,MDA含量显著上升(均P<0.01);与模型组相比,黄芪多糖组肝组织SOD活性明显升高(P<0.01),MDA含量明显降低(P<0.05)。与假手术组相比,模型组和黄芪多糖组肝组织IL-1β、TNF-α、IL-10水平显著升高(均P<0.01);与模型组相比,黄芪多糖组肝组织IL-1β、TNF-α明显降低,IL-10水平明显升高(均P<0.01)。与假手术组比较,模型组、黄芪多糖组肝组织HO-1表达明显上升(均P<0.01);与模型组比较,黄芪多糖组肝组织HO-1表达显著升高(P<0.01)。结论:黄芪多糖具有显著改善大鼠肝脏缺血再灌注损伤的作用,其机制可能与上调HO-1蛋白在肝脏组织中的表达,抑制促炎因子、发挥抗氧自由基作用以及促进抗炎因子的生成有关。

Objective:To observe the effect of Astragalus Polysaccharide(APS)on hepatic ischemia reperfusion injury in rats and explore its porentional mechanism.Methods:Thirty rats were divided into sham group,model group and APS group.The APS group was preoperatively administered,APS injection 30 mL·kg-1 was caudal vein injection each day for 7 days.The sham group and model group were given the same volume of sodium chloride injection.70%rat model of hepatic ischemia reperfusion injury was establishied,ALT,AST and LDH were measured at the 4 h after hepatic reperfution post 1 h ischemia.Liver tissues were gathered for SOD and MDA determination at various intervals.Contents of IL-1β,TNF-αand IL-10 in hepar were detected by ELISA.Expression level of HO-1 in rat liver tissue were detected by immunohistochemistry.Results:Compared with the model group,the content of serum ALT,AST,LDH and the content of MDA in hepar of APS group were significantly decreased(P<0.05,P<0.01),the activity of SOD in hepar of APS group were significantly increased(P<0.01);the level of IL-1β,TNF-αin hepar of APS group were significantly decreased,the level of IL-10 in hepar of APS group were significantly increased(P<0.01);the HO-1 expression l in hepar of APS group were significantly improved(P<0.01).Conclusion:APS has significantly improved effect of hepatic ischemia reperfusion injury in rats,and its mechanism may be related to the up-regulation of HO-1 protein expression,the decrease of the level of proinflammatory factors and the promotion of the release of anti-inflammatory factors.