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Evidence-Based Complementary and Alternative Medicine
Volume 2011, Article ID 803015, 9 pages
http://dx.doi.org/10.1155/2011/803015
Research Article

Neuroprotection by the Traditional Chinese Medicine, Tao-Hong-Si-Wu-Tang, against Middle Cerebral Artery Occlusion-Induced Cerebral Ischemia in Rats

1Division of Nephrology, Mackay Memorial Hospital, Taipei 104, Taiwan
2Mackay Medicine, Nursing and Management College, Taipei 112, Taiwan
3Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wuxing St., Taiwan
4Department of Anesthesiology, WanFang Hospital, and Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei 110, Taiwan

Received 20 May 2010; Revised 24 August 2010; Accepted 7 October 2010

Copyright © 2011 Chih-Jen Wu 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

Tao-Hong-Si-Wu-Tang (THSWT) is a famous traditional Chinese medicine (TMC). In the present study, oral administration of THSWT (0.7 and 1.4 g ) for 14 days before MCAO dose-dependently attenuated focal cerebral ischemia in rats. MCAO-induced focal cerebral ischemia was associated with increases in hypoxia-inducible factor (HIF)-1 , inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)- , and active caspase-3 expressions in ischemic regions. These expressions were obviously inhibited by 0.7 g THSWT treatment. In addition, THSWT inhibited platelet aggregation stimulated by collagen in washed platelets. In an in vivo study, THSWT (16 g ) significantly prolonged platelet plug formation in mice. However, THSWT (20 and 40  g ) did not significantly reduce the electron spin resonance (ESR) signal intensity of hydroxyl radical ( ) formation. In conclusion, the most important findings of this study demonstrate for the first time that THSWT possesses potent neuroprotective activity against MCAO-induced focal cerebral ischemia in vivo. This effect may be mediated, at least in part, by the inhibition of both HIF-1 and TNF- activation, followed by the inhibition of inflammatory responses (i.e., iNOS expression), apoptosis formation (active caspase-3), and platelet activation, resulting in a reduction in the infarct volume in ischemia-reperfusion brain injury.