雷帕霉素通过诱导细胞自噬增强乙肝病毒的产生。
Rapamycin enhances HBV production by inducing cellular autophagy.
作者信息
Huang Wenjuan, Zhao Fengrong, Huang Ying, Li Xia, Zhu Sufei, Hu Qin, Chen Weixian
机构信息
Department of Laboratory Medicine, Affiliated to the Second Hospital Chongqing Medical University, Chongqing, China.
Department of Gynaecology and Obstetrics, Youyang People's Hospital, Chongqing, China.
出版信息
Hepat Mon. 2014 Oct 15;14(10):e20719. doi: 10.5812/hepatmon.20719. eCollection 2014 Oct.
BACKGROUND
Some reports revealed that rapamycin could reactivate HBV infection. However, the mechanism has not been clearly explained.
OBJECTIVES
In this report, we studied the mechanism by which rapamycin enhances HBV replication and expression by inducing cellular autophagy.
MATERIALS AND METHODS
HepG2.2.15 cells were treated with rapamycin to induce autophagy. Autophagosomes were observed by fluorescence microscopy and transmission electron microscopy. Autophagy marker protein LC3-Ⅱ/LC3-Ⅰwas detected by Western blotting. HBV DNA and mRNA were determined by real time PCR and Southern blotting. HBsAg was evaluated by ELISA.
RESULTS
In HepG2.2.15 cells, HBV DNA and HBsAg increased when host cells were treated with rapamycin and the effect was reversed by autophagy inhibitor, 3-methyladenine (3-MA).
CONCLUSIONS
These results indicated a potential explanation for reactivation of HBV infection when patients with hepatitis receive rapamycin.
背景
一些报告显示雷帕霉素可重新激活HBV感染。然而，其机制尚未得到明确解释。
目的
在本报告中，我们研究了雷帕霉素通过诱导细胞自噬增强HBV复制和表达的机制。
材料与方法
用雷帕霉素处理HepG2.2.15细胞以诱导自噬。通过荧光显微镜和透射电子显微镜观察自噬体。通过蛋白质免疫印迹法检测自噬标记蛋白LC3-Ⅱ/LC3-Ⅰ。通过实时PCR和Southern印迹法测定HBV DNA和mRNA。通过ELISA评估HBsAg。
结果
在HepG2.2.15细胞中，当宿主细胞用雷帕霉素处理时，HBV DNA和HBsAg增加，并且自噬抑制剂3-甲基腺嘌呤（3-MA）可逆转该效应。
结论
这些结果为肝炎患者接受雷帕霉素治疗时HBV感染重新激活提供了一种可能的解释。
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