详细记录  
题名:Emodin blocks the SARS coronavirus spike protein and angiotensin-converting enzyme 2 interaction
作者:Tin-Yun Ho, Shih-Lu Wu, Jaw-Chyun Chen, Chia-Cheng Li and Chien-Yun Hsiang
来源:Antiviral Research[IF=3.406], Volume 74, Issue 2, May 2007, Pages 92-101
URL :http://dx.doi.org/10.1016/j.antiviral.2006.04.014
日期:070415
摘要: Tin-Yun Hoa, Shih-Lu Wub, Jaw-Chyun Chenc, Chia-Cheng Lid and Chien-Yun Hsiangd, ,

aMolecular Biology Laboratory, Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan
bDepartment of Biochemistry, China Medical University, Taichung, Taiwan
cGraduate Institute of Chinese Pharmaceutical, China Medical University, Taichung, Taiwan
dDepartment of Microbiology, China Medical University, 91 Hsueh-Shih Road, Taichung 404, Taiwan
Received 9 January 2006; accepted 11 April 2006. Available online 15 May 2006.

Summary

Severe acute respiratory syndrome (SARS) is an emerging infectious disease caused by a novel coronavirus (SARS-CoV). SARS-CoV spike (S) protein, a type I membrane-bound protein, is essential for the viral attachment to the host cell receptor angiotensin-converting enzyme 2 (ACE2). By screening 312 controlled Chinese medicinal herbs supervised by Committee on Chinese Medicine and Pharmacy at Taiwan, we identified that three widely used Chinese medicinal herbs of the family Polygonaceae inhibited the interaction of SARS-CoV S protein and ACE2. The IC50 values for Radix et Rhizoma Rhei (the root tubers of Rheum officinale Baill.), Radix Polygoni multiflori (the root tubers of Polygonum multiflorum Thunb.), and Caulis Polygoni multiflori (the vines of P. multiflorum Thunb.) ranged from 1 to 10 g/ml. Emodin, an anthraquinone compound derived from genus Rheum and Polygonum, significantly blocked the S protein and ACE2 interaction in a dose-dependent manner. It also inhibited the infectivity of S protein-pseudotyped retrovirus to Vero E6 cells. These findings suggested that emodin may be considered as a potential lead therapeutic agent in the treatment of SARS. 4.

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