榆干离褶伞溶栓酶对脂多糖诱导的大鼠炎性肝损伤的保护作用

刘雪; 王玉娇; 沈明花

doi:10.13386/j.issn1002-0306.2018.20.049

榆干离褶伞溶栓酶对脂多糖诱导的大鼠炎性肝损伤的保护作用

Protective Effects of Fibrinolytic Enzyme of Lyophyllum ulmarium on LPS-Induced Liver Injury in Rats

摘要

摘要: 本实验研究榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)对脂多糖(LPS)诱导的大鼠肝损伤的保护作用,并初步探讨其作用机制。将大鼠随机分为五组,分别为对照组、模型组、阳性对照组、LUFE低剂量组、LUFE高剂量组。LUFE分别以200、400 mg/kg体质量灌胃2周。除对照组以外其余四组均以腹腔注射LPS诱导大鼠肝脏炎性损伤模型。阳性对照组在造模前腹腔注射地塞米松(5 mg/kg)。苏木精-伊红(HE)染色观察肝组织病理改变;检测血清肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、白介素-1β(IL-1β)、丙氨酸氨基转移酶(ALT)、白蛋白(ALB)和天冬氨酸氨基转移酶(AST)的水平;Western bolt方法观察肝组织Toll样受体4(Toll like receptor 4,TLR4)、p-TAK1和p-NF-κB p65蛋白水平。实验结果表明,LUFE可缓解LPS诱导的肝组织的炎性损伤,降低血清TNF-α、IL-6、IL-1β含量和AST、ALT活性,提高ALB水平。Western bolt结果显示,LUFE下调TLR4、p-TAK1、p-NF-κBp65蛋白水平。以上结果表明LUFE抑制肝脏炎性损伤,其机制可能与其下调TLR4-NF-κB通路相关蛋白的表达有关。

Abstract: To observe the protective effects of fibrinolytic enzyme of Lyophyllum ulmarium (LUFE) in rats with liver injury induced by lipopolysaccharide (LPS). The rats were randomly divided into five groups:the normal control, model, positive control, and the low-and high-dose LUFE groups.Rats in the low-and high-dose LUFE groups were i.g given LUFE at dose of 200 and 400 mg/kg for a period of 2 weeks.Besides the control group, other four groups were i.p given lipopolysaccharide to induce inflammatory liver injury in rats.The positive control rats were i.p given 5 mg/kg dexamethasone before the model establishment.The morphological changes of liver were observed by light microscope.The levels of TNF-α, IL-6, IL-1β, ALT, AST and ALB in serum were measured.The expression of TLR4, p-TAK1 and NF-κB proteins was detected by Western blot. The results showed that LUFE could reduce the inflammatory damage in liver tissue, decrease the serum levels of TNF-α, IL-6, IL-1β, ALT, AST, increased the serum ALB, and down-regulate the expression of TLR4, p-TAK1 and p-NF-κB proteins in rats with liver injury.The above results indicated that LUFE had protective effects on the liver injury in rats.The effects may be related to the regulation of TLR4-NF-κB signaling pathway.