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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 232789, 8 pages
Research Article

Antrodia camphorata Potentiates Neuroprotection against Cerebral Ischemia in Rats via Downregulation of iNOS/HO-1/Bax and Activated Caspase-3 and Inhibition of Hydroxyl Radical Formation

1Department of Surgery, Mackay Memorial Hospital and Mackay Medical College, Taipei, Taiwan
2Department of Pharmacology, School of Medicine, Taipei Medical University, Taipei, Taiwan
3Cardiovascular Division, Department of Surgery, Yuan’s General Hospital, Kaohsiung, Taiwan
4Department of Cardiology, Cathay General Hospital, Taipei, Taiwan
5Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan
6Sheen Chain Biotechnology, Co., Ltd., Taipei, Taiwan

Received 28 August 2014; Accepted 20 October 2014

Academic Editor: Joen-Rong Sheu

Copyright © 2015 Po-Sheng Yang 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.


Antrodia camphorata (A. camphorata) is a fungus generally used in Chinese folk medicine for treatment of viral hepatitis and cancer. Our previous study found A. camphorata has neuroprotective properties and could reduce stroke injury in cerebral ischemia animal models. In this study, we sought to investigate the molecular mechanisms of neuroprotective effects of A. camphorata in middle cerebral artery occlusion (MCAO) rats. A selective occlusion of the middle cerebral artery (MCA) with whole blood clots was used to induce ischemic stroke in rats and they were orally treated with A. camphorata (0.25 and 0.75 g/kg/day) alone or combined with aspirin (5 mg/kg/day). To provide insight into the functions of A. camphorata mediated neuroprotection, the expression of Bax, inducible nitric oxide synthase (iNOS), haem oxygenase-1 (HO-1), and activated caspase-3 was determined by Western blot assay. Treatment of aspirin alone significantly reduced the expressions of HO-1 (), iNOS (), and Bax () in ischemic regions. The reduction of these expressions was more potentiated when rats treated by aspirin combined with A. camphorata (0.75 g/kg/day). Combination treatment also reduced apoptosis as measured by a significant reduction in active caspase-3 expression in the ischemic brain compared to MCAO group (). Moreover, treatment of A. camphorata significantly () reduced fenton reaction-induced hydroxyl radical (OH) formation at a dose of 40 mg/mL. Taken together, A. camphorata has shown neuroprotective effects in embolic rats, and the molecular mechanisms may correlate with the downregulation of Bax, iNOS, HO-1, and activated caspase-3 and the inhibition of OH signals.