保肝I号对D-氨基半乳糖和脂多糖致小鼠急性肝损伤的保护作用研究
The Protective Effects of BGYH on Mice Acute Liver Injury Induced by D-Galn and LPS
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摘要: 采用D-氨基半乳糖(D-GalN)联合脂多糖(LPS)诱导的小鼠急性肝损伤模型对保肝I号(BGYH)的保肝降酶及其可能机制进行研究.将小鼠随机分为正常对照组,模型组,BGYH低、中、高剂量组,水飞蓟素组和联苯双酯组.每天给药1次,连续9 d,末次给药后除正常组均腹腔注射D-GalN/LPS建立急性肝损伤模型.结果显示高剂量BGYH可以显著降低小鼠血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,同时,肝组织切片观察结果表明高剂量BGYH使小鼠肝细胞坏死程度有所减轻.在细胞因子方面,中或高剂量BGYH均可明显降低肿瘤坏死因子(TNF-α)及白细胞介素6(IL-6)等炎性细胞因子的表达,并同时升高抗炎因子白细胞介素(IL-10)的含量.此外,小鼠肝脏中一氧化氮(NO)、诱导性一氧化氮合酶(iNOS)水平在给予BGYH后也有下降的趋势.研究结果表明,BGYH对D-GalN和LPS联合诱导的小鼠急性肝损伤具有保护作用,可能是通过抑制免疫因子的释放,调节免疫反应而实现.Abstract: In the present study, D-GalN/LPS-induced acute liver injury mice model was applied to investigate the effectiveness of hepato-protective and descending transaminase function of BGYH. ICR mice were randomly divided into seven groups: control group, model group, low-, medium- and high-dose BGYH group, silymarin group and bifendate group. All dose groups were orally administrated respective drugs once for one day and continued for 9 days while control and model groups were given equal volume of vehicle. Post the last administration, D-GalN/LPS were injected intraperitoneally into mice except control group. The results show that the levels of ALT and AST in serum are significantly reduced in high-dose BGYH group. Meanwhile, sections of liver tissue also illustrated high-dose BGYH can alleviate necrocytosis of hepatocytes. Moreover, in the mechanism study, significant reduction of TNF-α and IL-6 in serum of medium- and high- dose BGYH group is observed, and concentration of IL-10 is remarkably increased. Furthermore, declining trend of NO and iNOS concentration occures in liver tissue. In conclusion, BGYH possessed protective effects on mice acute liver injury induce by D-GalN/LPS through the immunomodulation pathway.
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