KIZ OpenIR  > 科研部门  > 分子免疫药理学(郑永唐)
Trichosanthin suppresses the elevation of p38 MAPK, and Bcl-2 induced by HSV-1 infection in Vero cells
Huang H1; Chan H1; Wang YY2,3; Ouyang DY2,3; Zheng YT2; Tam SC*1; mtam@cuhk.edu.hk
2006
发表期刊LIFE SCIENCES
ISSN0024-3205
卷号79期号:13页码:1287-1292
合作性质其它
摘要Trichosanthin (TCS) is a type I ribosome-inactivating protein (RIP) effective against HIV-1 and HSV-1 replication. The mechanism of its antiviral activity is not clear. Many believe that it is related to ribosome inactivation. Some RIPs and viral infection affect the phosphorylation of MAPK and Bcl-2 and these proteins may be the common element linking RIP and viral infection. This study investigated the effect of HSV-1 infection on p38 MAPK and Bcl-2 as well as possible interference by TCS. Results showed that HSV-1 infection induced an elevation of phosphorylated p38 and Bcl-2 in Vero cells, which could be partially blocked by TCS. At the same time, both viral replication and host cells viability were lowered. Viral replication, Vero cell viability, p38 MAPK and Bcl-2 were further reduced with the addition of a p38 MAPK inhibitor (SB203580). This suggested that TCS may interfere with MAPK and Bcl-2 signals generated by infection leading to inhibition of viral replication. In summary, our results demonstrated that HSV-1 infection in Vero cells induced an elevation of p38 MAPK and Bcl-2. TCS suppressed this rise and reduced viral replication. The MAPK family may play a role in the antiviral mechanism of TCS.
关键词Trichosanthin Hsv-1 Mapk Bcl-2 Antiviral Activity
资助者The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142).
URL查看原文
收录类别SCI
资助者The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142). ; The work was supported by grants from the Natural Science Foundation of China (39970851) and Yunnan Province (2002C0066M); CAS Knowledge Innovation Projects (KSCX2-SW-216), Key Scientific and Technological Projects of China (2004BA719A14) and Yunnan Province (2004NG12), and 863 Program (2003AA219142).
文献类型期刊论文
条目标识符http://ir.kiz.ac.cn/handle/152453/4557
专题科研部门_分子免疫药理学(郑永唐)
通讯作者mtam@cuhk.edu.hk
作者单位1.Department of Physiology, The Chinese University of Hong Kong, Hong Kong SAR, China
2.Laboratory of Molecular Immunopharmacology, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China
3.Graduate School of the Chinese Academy of Sciences, Beijing 100039, China
推荐引用方式
GB/T 7714
Huang H,Chan H,Wang YY,et al. Trichosanthin suppresses the elevation of p38 MAPK, and Bcl-2 induced by HSV-1 infection in Vero cells[J]. LIFE SCIENCES,2006,79(13):1287-1292.
APA Huang H.,Chan H.,Wang YY.,Ouyang DY.,Zheng YT.,...&mtam@cuhk.edu.hk.(2006).Trichosanthin suppresses the elevation of p38 MAPK, and Bcl-2 induced by HSV-1 infection in Vero cells.LIFE SCIENCES,79(13),1287-1292.
MLA Huang H,et al."Trichosanthin suppresses the elevation of p38 MAPK, and Bcl-2 induced by HSV-1 infection in Vero cells".LIFE SCIENCES 79.13(2006):1287-1292.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
2006791287.pdf(260KB)期刊论文出版稿开放获取CC BY-NC-SA请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Huang H]的文章
[Chan H]的文章
[Wang YY]的文章
百度学术
百度学术中相似的文章
[Huang H]的文章
[Chan H]的文章
[Wang YY]的文章
必应学术
必应学术中相似的文章
[Huang H]的文章
[Chan H]的文章
[Wang YY]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。