敲除FcεR1加重小鼠非酒精性脂肪肝病

基础医学与临床 ›› 2016, Vol. 36 ›› Issue (7): 946-950.

敲除FcεR1加重小鼠非酒精性脂肪肝病

崔杏杏¹,李瑶²,任梦²,张孝国¹,张琨¹,陈士俊³,王婧²

1. 山东大学济南市传染病医院
2. 中国医学科学院基础医学研究所
3. 济南市传染病医院

收稿日期:2016-03-03 修回日期:2016-05-23 出版日期:2016-07-05 发布日期:2016-06-22
通讯作者: 王婧 E-mail:wangjing@ibms.pumc.edu.cn
基金资助:
国家自然科学基金

Deficiency of FcεR1 aggravates NAFLD in mice

Received:2016-03-03 Revised:2016-05-23 Online:2016-07-05 Published:2016-06-22
Contact: Jing WANG E-mail:wangjing@ibms.pumc.edu.cn

摘要/Abstract

摘要： 目的探讨IgE高亲和力受体FcεR1在高脂饮食（HFD）诱导的小鼠非酒精性脂肪肝病（NAFLD）中的作用。方法选取野生型（WT）雄鼠和IgE高亲和力受体FcεR1敲除（FcεR1-/-）雄鼠各10只，均给予HFD诱导NAFLD模型，每周固定时间称取小鼠体质量。12周后处死小鼠，称取小鼠体质量，收取血及肝组织并检测肝功能相关指标。结果 FcεR1-/-小鼠与WT小鼠相比，体质量增加的同时（P＜0.05），肝脏体重比增高（P＜0.05），血清中天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、三酰甘油（TG）、总胆固醇（CHOL）及肝组织TG均升高（P＜0.01），肝组织III型胶原（collagen III）mRNA表达升高（P＜0.01），NAFLD症状严重。结论 IgE高亲和力受体FcεR1可能具有保护NAFLD诱导肝损伤的作用，其机制可能是通过降低体质量和改善脂质代谢实现的。

关键词: 关键词：IgE, FcεR1, 非酒精性脂肪肝病, 肝功能

Abstract: Objective To study the role of IgE high affinity receptor FcεR1 on HFD-induced non-alcoholic fatty liver disease (NAFLD) in mice. Methods To induce NAFLD, both WT and FcεR1-/- mice from each group (n=10, male) were fed with a high fat western diet for 12 weeks. Body weight was measured at a fixed time every week. All mice were sacrificed after 12 weeks treatment. Serum and liver were harvested to examine liver relevant parameters. Results Compared with WT mice, body weight and liver/body ratio in FcεR1-/- mice were increased (P<0.05). Meanwhile, serum AST and ALT, blood lipids (including TG, CHOL), hepatic TG and hepatic Collagen III mRNA levels were also significantly elevated in FcεR1-/- mice(P<0.01), indicating a more severe NAFLD symptom. Conclusions IgE high affinity receptor FcεR1 may have a protective effect on HFD-induced NAFLD,the mechanism may be reducing body weight and improving lipid metabolism.

Key words: Key words: IgE, FcεR1, NAFLD, Liver function

中图分类号:

575.5

崔杏杏李瑶任梦张孝国张琨陈士俊王婧. 敲除FcεR1加重小鼠非酒精性脂肪肝病[J]. 基础医学与临床, 2016, 36(7): 946-950.