期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 279, 期 3, 页码 294-302出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2014.07.005
关键词
Magnolol; Stroke animal model; Inducible NO synthase; p38 mitogen-activated protein kinases; Akt; NF-kappa B
资金
- Cathay General Hospital [CGH-MR-9913]
- National Yang-Ming University Hospital [RD2011008]
- Chang Gung Memorial Hospital-Kaohsiung Medical Center [CZRPG880253]
- Chang Gung Memorial Hospital [CMRPF6A0073]
- Chang Gung University of Science and Technology, Chia-Yi Campus, Taiwan [CMRPF6C0032]
- National Science Council, Taiwan [NSC102-2113-M-010-001-MY3, NSC101-2622-B-255-001-CC3, NSC102-2313-B-255-002]
- Taipei City Hospital, Taipei, Taiwan [TCH 103-02, TCH 10301-62-021]
Magnolol is isolated from the herb Magnolia officinalis, which has been demonstrated to exert pharmacological effects. Our aim was to investigate whether magnolol is able to act as an anti-inflammatory agent that brings about neuroprotection using a global ischemic stroke model and to determine the mechanisms involved. Rats were treated with and without magnolol after ischemia reperfusion brain injury by occlusion of the two common carotid arteries. The inflammatory cytokine production in serum and the volume of infarction in the brain were measured. The proteins present in the brains obtained from the stroke animal model (SAM) and control animal groups with and without magnolol treatment were compared. Magnolol reduces the total infarcted volume by 15% and 30% at dosages of 10 and 30 mg/kg, respectively, compared to the untreated SAM group. The levels of acute inflammatory cytokines, including interleukin-1 beta, tumor necrosis factor alpha, and interleukin-6 were attenuated by magnolol. Magnolol was also able to suppress the production of nitrotyrosine, 4-hydroxy-2-nonenal (4-HNE), inducible NO synthase (iNOS), various phosphorylated p38 mitogen-activated protein kinases and various C/EBP homologues. Furthermore, this modulation of ischemia injury factors in the SAM model group treated with magnolol seems to result from a suppression of reactive oxygen species production and the upregulation of p-Akt and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B). These findings confirm the anti-oxidative properties of magnolol, including the inhibition of ischemic injury to neurons; this protective effect seems to involve changes in the in vivo activity of Akt, GSK3 beta and NF-kappa B. (C) 2014 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据