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目的研究免疫性肝损伤中结构型（ｃＮＯＳ）、诱导型（ｉＮＯＳ）一氧化氮合酶及凋亡相关基因Ｂａｘ、Ｂｃｌ－２表达的变化，在进一步探讨免疫性肝损伤机制的同时观察当归多糖的干预调控作用。方法建立卡介苗和脂多糖诱导的小鼠免疫性肝损伤模型，给予当归多糖 ３０ ｍｇ／ｋｇ、 ６０ ｍｇ／ｋｇ，测定血中 ＡＬＴ、 ＧＳＴ活性及肝中 ＮＯ含量；用免疫组织化学方法观察ｃＮＯＳ、ｉＮＯＳ、Ｂａｘ、Ｂｃｌ－２的表达。结果免疫性肝损伤小鼠ｓＡＬＴ、ｓＧＳＴ及ＮＯ含量明显升高，ｉＮＯＳ含量为正常鼠的１７．８倍，ｃＮＯＳ无明显变化，抗调亡基因Ｂｃｌ－２呈阴性表达，而具有启动凋亡信号、抑制Ｂｃｌ－２表达的 Ｂａｘ增加３１．１％。小剂量当归多糖可使 ｓＡＬＴ、 ｓＧＳＴ及 ＮＯ含量分别降低 ２４．６％、 ４０．８％、 １８．４％， ｉＮＯＳ、Ｂａｘ表达下降８４．２％、 ３７．１％，并使ｃＮＯＳ表达升高６６．８％， Ｂｃｌ－２表达增加 ３．３８倍；大剂量当归多糖可使ｓＡＬＴ、 ｓＧＳＴ及ＮＯ含量分别降低３６．６％、３４．５％、１６、９％，对Ｂａｘ表达的降低作用及对ｃＮＯＳ、Ｂｃｌ－２表达的增加作用不及小剂量明显，但能明显地降低ｉＮＯＳ的表达。结论肝中ＮＯ含量的变
Objective To study the changes of constitutive (cNOS), inducible nitric oxide synthase (iNOS) and apoptosis-related genes Bax and Bcl-2 in autoimmune liver injury. To further explore the mechanism of immune liver injury, The role of intervention in regulation. Methods The animal models of immune liver injury induced by BCG and lipopolysaccharide were established. Angelica polysaccharide 30 mg / kg and 60 mg / kg were given respectively. ALT, GST activity and NO content in liver were measured. Immunohistochemistry was used to observe the expression of cNOS, iNOS, Bax, Bcl-2 expression. Results The levels of sALT, sGST and NO in immunological liver injury mice were significantly increased, the content of iNOS was 17.8 times that of normal mice, cNOS had no obvious change, anti-apoptosis gene Bcl-2 was negative, , Bax, which inhibits the expression of Bcl-2, increased by 31.1%. Low-dose Angelica sinensis polysaccharide can reduce sALT, sGST and NO content by 24.6%, 40.8% and 18.4%, respectively. The expression of iNOS and Bax decreased by 84.2% and 37.1%, and the expression of cNOS increased 66.8% and Bcl-2 increased by 3.38-fold. High-dose Angelica sinensis polysaccharide reduced the levels of sALT, sGST and NO by 36.6%, 34.5% and 16.9%, respectively, And the increase of cNOS and Bcl-2 expression was less than the small dose, but it could obviously reduce the expression of iNOS. Conclusion The change of NO content in liver