Table of Contents Author Guidelines Submit a Manuscript
Mediators of Inflammation
Volume 2006, Article ID 30490, 9 pages
http://dx.doi.org/10.1155/MI/2006/30490
Research Communication

Theaflavin Ameliorates Cerebral Ischemia-Reperfusion Injury in Rats Through Its Anti-Inflammatory Effect and Modulation of STAT-1

1Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
2Department of Pharmacology, Medical College, Xianning University, 3 Guihua Road, Xianning 437100, China
3Department of Pharmacology, Medical College, Wuhan University, 39 Donghu Road, Wuhan 430071, China

Received 30 March 2006; Revised 30 August 2006; Accepted 30 August 2006

Copyright © 2006 Fei Cai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Theaflavin, a major constituent of black tea, possesses biological functions such as the antioxidative, antiviral, and anti-inflammatory ones. The purpose of this study was to verify whether theaflavin reduces focal cerebral ischemia injury in a rat model of middle cerebral artery occlusion (MCAO). Male Sprague-Dawley rats were anesthetized and subjected to 2 hours of MCAO followed 24 hours reperfusion. Theaflavin administration (5, 10, and 20 mg/kg, IV) ameliorated infarct and edema volume. Theaflavin inhibited leukocyte infiltration and expression of ICAM-1, COX-2, and iNOS in injured brain. Phosphorylation of STAT-1, a protein which mediates intracellular signaling to the nucleus, was enhanced 2-fold over that of sham group and was inhibited by theaflavin. Our study demonstrated that theaflavin significantly protected neurons from cerebral ischemia-reperfusion injury by limiting leukocyte infiltration and expression of ICAM-1, and suppressing upregulation of inflammatory-related prooxidative enzymes (iNOS and COX-2) in ischemic brain via, at least in part, reducing the phosphorylation of STAT-1.