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Int. J. Mol. Sci. 2014, 15(9), 15073-15089; doi:10.3390/ijms150915073

Protective Effects of Hericium erinaceus Mycelium and Its Isolated Erinacine A against Ischemia-Injury-Induced Neuronal Cell Death via the Inhibition of iNOS/p38 MAPK and Nitrotyrosine

1
Department of Pathology, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
2
Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan
3
School of Medicine, Fu-Jen Catholic University, Taipei 24205, Taiwan
4
Department of Emergency Medicine, Cathay General Hospital, Taipei 22174, Taiwan
5
Department of Nursing and Chronic Diseases and Health Promotion Research Center, Chang Gung University of Science and Technology, Chiayi 61363, Taiwan
6
Department of Hepato-Gastroenterology, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
7
Division of Colon and Rectal Surgery, Department of Surgery, Chang Gung Memorial Hospital, Chiayi 61363, Taiwan
8
Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan 330, Taiwan
9
Department of Colorectal Surgery and Department of Surgery, Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan
10
Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung 833, Taiwan
11
Grape King Biotechnology Inc., Zhong-Li 320, Taiwan
12
Department of Nursing, Chang Gung University of Science and Technology, Chiayi 61363, Taiwan
13
Chronic Diseases and Health Promotion Research Center, Chang Gung University of Science and Technology, Chiayi 61363, Taiwan
14
Research Center for Industry of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 333, Taiwan
*
Authors to whom correspondence should be addressed.
Received: 14 July 2014 / Revised: 15 August 2014 / Accepted: 19 August 2014 / Published: 27 August 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Hericium erinaceus, an edible mushroom, has been demonstrated to potentiate the effects of numerous biological activities. The aim of this study was to investigate whether H. erinaceus mycelium could act as an anti-inflammatory agent to bring about neuroprotection using a model of global ischemic stroke and the mechanisms involved. Rats were treated with H. erinaceus mycelium and its isolated diterpenoid derivative, erinacine A, after ischemia reperfusion brain injuries caused by the occlusion of the two common carotid arteries. The production of inflammatory cytokines in serum and the infracted volume of the brain were measured. The proteins from the stroke animal model (SAM) were evaluated to determine the effect of H. erinaceus mycelium. H. erinaceus mycelium reduced the total infarcted volumes by 22% and 44% at a concentration of 50 and 300 mg/kg, respectively, compared to the SAM group. The levels of acute inflammatory cytokines, including interleukin-1β, interleukin-6 and tumor necrosis factor á, were all reduced by erinacine A. Levels of nitrotyrosine-containing proteins, phosphorylation of p38 MAPK and CCAAT enhancer-binding protein (C/EBP) and homologous protein (CHOP) expression were attenuated by erinacine A. Moreover, the modulation of ischemia injury factors present in the SAM model by erinacine A seemed to result in the suppression of reactive nitrogen species and the downregulation of inducible NO synthase (iNOS), p38 MAPK and CHOP. These findings confirm the nerve-growth properties of Hericium erinaceus mycelium, which include the prevention of ischemic injury to neurons; this protective effect seems to be involved in the in vivo activity of iNOS, p38 MAPK and CHOP. View Full-Text
Keywords: Hericium erinaceus; neuroprotection; erinacine A; ischemia reperfusion; iNOS Hericium erinaceus; neuroprotection; erinacine A; ischemia reperfusion; iNOS
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MDPI and ACS Style

Lee, K.-F.; Chen, J.-H.; Teng, C.-C.; Shen, C.-H.; Hsieh, M.-C.; Lu, C.-C.; Lee, K.-C.; Lee, L.-Y.; Chen, W.-P.; Chen, C.-C.; Huang, W.-S.; Kuo, H.-C. Protective Effects of Hericium erinaceus Mycelium and Its Isolated Erinacine A against Ischemia-Injury-Induced Neuronal Cell Death via the Inhibition of iNOS/p38 MAPK and Nitrotyrosine. Int. J. Mol. Sci. 2014, 15, 15073-15089.

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