摘要
目的:探索在四氯化碳诱导小鼠肝纤维化形成过程中,核因子相关因子2(Nrf2)对炎症细胞浸润的影响。方法:野生鼠和Nrf2基因敲除鼠各24只,分别随机平均分成对照组和模型组。HE染色、Masson三色染色观察肝组织病理学变化及肝脏纤维化程度;天狼星红染色观察胶原沉积情况;免疫组化方法检测肝组织中中性粒细胞浸润(Ly6-G阳性)情况;免疫荧光方法检测巨噬细胞浸润及活化(ER-MP23阳性)情况。结果:两个对照组均未有肝纤维化表现;基因敲除模型组小鼠肝组织坏死及纤维化程度重于野生模型组,胶原含量更多(P<0.05)。四氯化碳诱导可增强肝组织中中性粒细胞的浸润,但基因敲除鼠中性粒细胞浸润轻于野生模型鼠(P<0.05)。Nrf2基因敲除和四氯化碳诱导均增强肝组织中巨噬细胞的活化,两者具有协同效应(P<0.05)。结论:Nrf2可以通过抑制巨噬细胞活化抑制四氯化碳诱导的肝纤维化发展。
Aim： To investigate the effects of nuclear factor-E2 related factor 2（ Nrf2） on infiltration of inflammatory cells from rats with CCl4-induced liver fibrosis. Methods： There were four groups including wild type（ WT） control group（ WT mice without CCl4-induction）,WT-CCl4group（ WT mice with CCl4-induction）,Nrf2 knockout（ Nrf2^（-/-）） control group（ Nrf2^（-/-）mice without CCl4-induction） and Nrf2^（-/-）-CCl4group（ Nrf2^（-/-）mice with CCl4-induction）,and 12 in each group. Histological morphology was studied by HE staining,Masson triple staining,and Sirius red staining was used to observe the deposition of collagen. Neutrophils（ labelled by Ly6-G） and macrophages（ labelled by ER-MP23） infiltration were detected by immunohistochemical staining and immunofluorescence,respectively. Results： The two control groups had no liver fibrosis pathogenic manifestations; the liver fibrosis was more severe and collagen content was higher in Nrf2^（-/-）-CCl4 group than those in WT-CCl4group（ P〈0. 05）. In the WT-CCl4 group,the infiltration of neutrophils were increased obviously compared with control groups,but there was a significant decrease in the Nrf2^（-/-）-CCl4 group when compared with the WT-CCl4group（ P〈0. 05）. The macrophages were infiltrated and activated in the model groups than in the control groups,especially in the Nrf2^（-/-）-CCl4group（ P〈0. 05）. Conclusion： Nrf2 plays a protective role in CCl4-induced liver fibrosis via inhibiting the activation of macrophages.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2016年第3期337-341,共5页
Journal of Zhengzhou University(Medical Sciences)
