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学科主题: 药学
题名:
Anti-neuroinflammatory efficacy of the aldose reductase inhibitor FMHM via phospholipase C/protein kinase C-dependent NF-kappa B and MAPK pathways
作者: Zeng, Ke-Wu1; Li, Jun2; Dong, Xin1; Wang, Ying-Hong1; Ma, Zhi-Zhong1; Jiang, Yong1; Jin, Hong-Wei1; Tu, Peng-Fei1,2
关键词: Aldose reductase ; Protein kinase C ; Nuclear factor-kappa B (NF-kappa B) ; Neuroinflammation ; Microglia
刊名: TOXICOLOGY AND APPLIED PHARMACOLOGY
发表日期: 2013-11-15
DOI: 10.1016/j.taap.2013.08.028
卷: 273, 期:1, 页:159-171
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]: Pharmacology & Pharmacy ; Toxicology
关键词[WOS]: NERVE CONDUCTION-VELOCITY ; NEURODEGENERATIVE DISEASES ; PROTEIN-KINASE ; THERAPEUTIC AGENTS ; NITRIC-OXIDE ; INFLAMMATION ; MICROGLIA ; ACTIVATION ; RECEPTOR ; MACROPHAGES
英文摘要:

Aldose reductase (AR) has a key role in several inflammatory diseases: diabetes, cancer and cardiovascular diseases. Therefore, AR inhibition seems to be a useful strategy for anti-inflammation therapy. In the central nervous system (CNS), microglial over-activation is considered to be a central event in neuroinflammation. However, the effects of AR inhibition in CNS inflammation and its underlying mechanism of action remain unknown. In the present study, we found that FMHM (a naturally derived AR inhibitor from the roots of Polygala tricornis Gagnep.) showed potent anti-neuroinflammatory effects in vivo and in vitro by inhibiting microglial activation and expression of inflammatory mediators. Mechanistic studies showed that FMHM suppressed the activity of AR-dependent phospholipase C/protein kinase C signaling, which further resulted in downstream inactivation of the I kappa B kinase/I kappa B/nuclear factor-kappa B (NF-kappa B) inflammatory pathway. Therefore, AR inhibition-dependent NF-kappa B inactivation negatively regulated the transcription and expression of various inflammatory genes. AR inhibition by FMHM exerted neuroprotective effects in lipopolysaccharide-induced neuron-microglia co-cultures. These findings suggested that AR is a potential target for neuroinflammation inhibition and that FMHM could be an effective agent for treating or preventing neuroinflammatory diseases. (C) 2013 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: 2012ZX09301002-002-002 ; 81303253 ; 30873072 ; 2012M510294 ; 2013T60045
项目资助者: National Key Technology R &amp ; D Program "New Drug Innovation" of China ; Natural Science Foundation of China ; China Postdoctoral Science Foundation ; Postdoctoral Fellowship of Peking-Tsinghua Center for Life Sciences
WOS记录号: WOS:000327290000017
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64661
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
2.Beijing Univ Chinese Med, Modern Res Ctr Tradit Chinese Med, Beijing 100029, Peoples R China

Recommended Citation:
Zeng, Ke-Wu,Li, Jun,Dong, Xin,et al. Anti-neuroinflammatory efficacy of the aldose reductase inhibitor FMHM via phospholipase C/protein kinase C-dependent NF-kappa B and MAPK pathways[J]. TOXICOLOGY AND APPLIED PHARMACOLOGY,2013,273(1):159-171.
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