诱导型一氧化氮合酶在ConA诱发T细胞介导的小鼠肝损害中的表达

The expression of inducible nitric oxide synthase in T cell dependent liver injury in mice induced by concanavalin A

目的观察诱导型一氧化氮合酶（ｉＮＯＳ）在刀豆素Ａ（ＣｏｎＡ）诱发Ｔ细胞介导的小鼠肝损害中的表达及意义。方法应用黄递酶染色（ＮＡＤＰＨ－ｄ）技术观察ｉＮＯＳ表达。结果ＣｏｎＡ造成肝损害后，血浆中亚硝酸盐（ＮＯ－２）较正常对照组（ＰＢＳ组）显著升高，以Ｌ－ＮＡＭＥ抑制ＮＯ合成，肝细胞损害反而加重，且肝组织内丙二醛（ＭＤＡ）增加，肝窦内血细胞聚集加重；在ＣｏｎＡ造成肝损害时可见肝实质细胞表达ｉＮＯＳ，且越靠近中央静脉的肝细胞表达越多，推测这是肝细胞对缺血缺氧而产生的一种自身反映；用环孢霉素Ａ（ＣＳＡ）预先抑制Ｔ细胞活化，则未发现肝细胞表达ｉＮＯＳ。结论在ＣｏｎＡ性肝损害中，肝实质细胞通过启动自身的ＮＯ生物合成机制参与了炎症应答，并通过消除氧自由基和抑制血细胞在肝窦内聚集而起一定的保护作用，这一生物过程很可能是肝细胞参与机体免疫应答的一部分。

Objective To observe the expression and effect of inducible nitric oxide synthase (iNOS) in T cell dependent liver injury in mice initiated by concanavalin A(ConA).Methods Using NADPH diaphorase staining,we observed the expression of iNOS.Results Liver injury became more serious if NO synthesis was inhibited.The further study showed that the MDA in liver increased greatly and vascular thrombosis became more serious.We also found that the more near the hepatocytes closed to the central vein,the more iNOS was expressed,which may be due to the lack of sufficient supply of blood and oxygen.The expression of iNOS could not be observed if cyclosporine A(CSA)-an inhibitor of T lymphocyte was used before ConA challenging introvenously.Conclusions NO plays a protective role in ConA induced liver injury by eradicating oxygen radicals and inhibite intro vascular thrombosis,the trigger of NO biologic synthesis in hepatocyte during liver inflammatory process is the outcome of the activation of T cell.It is likely that the expression of iNOS is one part of the host immune response.