MHV-3诱导暴发性肝炎小鼠肝组织KCNJ15的表达变化*

doi:10.3969/j.issn.1672-5069.2012.04.021

实用肝脏病杂志 ›› 2012, Vol. 15 ›› Issue (4): 336-338.doi: 10.3969/j.issn.1672-5069.2012.04.021

MHV-3诱导暴发性肝炎小鼠肝组织KCNJ15的表达变化^*

朱琳, 陈韬, 王帅, 宁琴

430030 武汉市华中科技大学附属同济医院感染性疾病研究所/感染病科

收稿日期:2012-03-06 出版日期:2012-08-10 发布日期:2017-03-15
通讯作者: 宁琴，E-mail：qning@tjh.tjmu.edu.cn
作者简介:朱琳女，28岁，博士研究生。主要从事病毒性肝炎免疫发病机制研究
基金资助:
国家自然科学基金重点项目（No.81030007）；国家自然科学基金（No.81100308）

The hepatic expression of KCNJ15 in mice with MHV-3-induced fulminant hepatitis

Zhu Lin, Chen Tao, Wang Shuai, et al.

Institute and Department of Infectious Diseases,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China

Received:2012-03-06 Online:2012-08-10 Published:2017-03-15

摘要/Abstract

摘要： 目的研究病毒感染所致的急性肝衰竭模型中离子通道基因KCNJ15表达水平,探讨该疾病模型中KCNJ15的变化及其与疾病进程的关系。方法利用MHV-3病毒诱导的Balb/cJ小鼠暴发型肝炎模型,采用定量PCR和免疫组化技术分别从基因及蛋白水平检测肝脏KCNJ15表达水平,并应用流式细胞术检测肝脏淋巴细胞亚群KCNJ15表达。结果随着MHV-3感染时间的延长,肝组织中KCNJ15表达水平逐渐增高,以感染后72小时最为显著。在肝脏CD4⁺T细胞,KCNJ15蛋白表达水平于48小时显著升高,达到25.17±7.68%,与0h（3.92±1.33%）相比差异具有统计学意义（P<0.001）,随后于72小时回落;肝脏表达KCNJ15的CD8⁺T细胞比例变化与CD4⁺T细胞趋势一致,于48h达到37.08±8.73%,与0h（6.98±3.48%）相比有显著差异（P<0.001）;而表达KCNJ15的肝脏NK细胞比例则从7.72±1.34%上升到感染后24小时的峰值19.80±4.25%（P<0.001）,随后回落。结论肝组织及肝脏淋巴细胞过表达KCNJ15可能参与了MHV-3诱导的暴发性肝炎小鼠免疫诱导的肝脏损伤过程。

关键词: 暴发性肝炎, KCNJ15, MHV-3, Balb/cJ小鼠

Abstract: Objective To investigate the hepatic expression of KCNJ15 in mice with MHV-3-induced fulminant hepatitis. Method MHV-3-induced fulminant hepatitis model was established and the hepatic expression of KCNJ15 were assayed by quantitative PCR and immunohistochemistry. KCNJ15 expressions on subgroups of intrahepatic lymphocytes were determined by flow cytometry. Results The enhanced expression of KCNJ15 in liver tissue was observed,especially at 72h after MHV-3 injection. Moreover,the percentage of KCNJ15-producing CD4⁺T cells in the liver at 48h post infection increased to 25.17±7.68%,which was remarkably higher than that of at 0h（3.92±1.33%,P<0.001）;Similarly,hepatic KCNJ15-producing CD8⁺T cells was also increased to 37.08±8.73% with a significant difference as comparing to that of at 0h（6.98±3.48%,P<0.001）;Meanwhile,hepatic NK cells expressed KCNJ15 increased significantly from 7.72±1.34% at 0h to 19.80±4.25% at 24h post infection（P<0.001）. Conclusion The increased expression of KCNJ15 in liver may correlate with immune regulatory function of hepatic lymphocytes,which contributes to virus induced liver failure.

朱琳, 陈韬, 王帅, 宁琴. MHV-3诱导暴发性肝炎小鼠肝组织KCNJ15的表达变化^*[J]. 实用肝脏病杂志, 2012, 15(4): 336-338.

Zhu Lin, Chen Tao, Wang Shuai, et al.. The hepatic expression of KCNJ15 in mice with MHV-3-induced fulminant hepatitis[J]. JOURNAL OF PRACTICAL HEPATOLOGY, 2012, 15(4): 336-338.

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MHV-3诱导暴发性肝炎小鼠肝组织KCNJ15的表达变化^*

The hepatic expression of KCNJ15 in mice with MHV-3-induced fulminant hepatitis

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