自身免疫性肝炎小鼠肝组织神经细胞粘附分子的表达

Expression of neural cell adhesion molecule in murine livers with experimental autoimmune hepatitis

目的观察实验性自身免疫性肝炎（ＥＡＨ）肝组织中神经细胞粘附分子（ＮＣＡＭ）的表达，并探讨其表达强度与肝组织学分级的相关性。方法以同种系Ｓ－１００肝抗原与弗氏完全佐剂充分乳化后于第１和第７大于Ｃ５７ＢＬ／６小鼠腹腔注射诱导ＥＡＨ模型。分别于首次免疫后第７、１４和２１天处死小鼠。以免疫组织化学和ＲＴ－ＰＣＲ 法研究ＮＣＡＭ表达。结果ＥＡＨ模型组小鼠肝内ＮＣＡＭ表达逐渐增强，淋巴细胞浸润和肝细胞破坏逐渐加重。强的松龙可改善肝组织学分级，并抑制ＮＣＡＭ的表达。ＮＣＡＭ的表达强度与肝组织学分级呈正相关（ｒ＝０．７１，Ｐ＜０．０１）。结论ＮＣＡＭ作为移行信号而便于淋巴细胞的肝内浸润，从而诱导肝细胞的损伤。

Objective To investigate the expression of neural cell adhesion molecule (NCAM) in murine livers with experimental autoimmune hepatitis (EAH) and its relationship with histological grades. Methods To induce the EAH model, the syngeneic S-100 antigen emulsified in complete Freud's adjuvant was injected intraperitoneally to C57B1/6 at day 1 and day 7. The mice were sacrificed at day 7, 14, and 21 after the first immunization. The expression of NCAM was observed using histoimmunochemistry and RT-PCR. Results The expression of NCAM increased gradually with aggravation of lymphocyte infiltration and hepatocyte injury. The administration of prednisolone decreased the histological grade, and inhibited the expression of NCAM. There was a correlation between the expression of NCAM and histological grade(r=0.71, p<0.01). Conclusions NCAM provides a traffic signal for infiltration of lymphocytes in the liver, hence induces the injury of hepatocytes.