中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
首页 机构 成果 学者
  
  1. CAS IR Grid
  2. 上海药物研究所
  3. 中国科学院上海药物研究所
  4. 药物化学研究室
LLDT-8 protects against cerebral ischemia/reperfusion injury by suppressing post-stroke inflammation

文献类型：期刊论文

作者Chen, Yanke1,4; Zhang, Li1,4; Ni, Jingshu1,4; Wang, Xiaoyu1,4; Cheng, Jian3,4; Li, Yuanchao2; Zhen, Xuechu1,4; Cao, Ting1,4; Jia, Jia1,4
刊名JOURNAL OF PHARMACOLOGICAL SCIENCES
出版日期2016-06
卷号131期号:2页码:131-137
关键词LLDT-8 Cerebral ischemia Neuroinflammation Microglia
ISSN号1347-8613
DOI10.1016/j.jphs.2016.05.003
文献子类Article
英文摘要Aim: (5R)-5-Hydroxytriptolide (LLDT-8), an analogue of triptolide, displays lower toxicity compared to triptolide and has comparable immunosuppressive effects. We investigated the anti-inflammatory and neuroprotective effects of LLDT-8 on cerebral ischemia/reperfusion injury. Methods: Nitric oxide production from microglia was assessed by measuring the nitrite concentration in the culture medium with Griess reagent. Microglial cells and ischemic brain tissues were examined for the expression of proinflammatory mediators by qPCR and western blot. Infarct volumes were assessed with TTC histology. The TLR4/NF-kappa B signaling pathway was analyzed with western blot and immunocytochemistry. Results: LLDT-8 significantly reduced infarct sizes and expression of pro-inflammatory cytokines in the ischemic cortex. LLDT-8 inhibited NO release and expression of TNF-alpha, IL-1 beta and iNOS in BV-2 microglia and primary microglia treated with LPS. In addition, LLDT-8 suppressed expression of TLR4, degradation of I kappa B alpha and nuclear translocation of NF-kappa B. Conclusion: LLDT-8 exerted anti-inflammatory effects and protected against acute cerebral ischemia/reperfusion injury possibly by acting through the I kappa B/NF-kappa B cascade to suppress microglia-mediated neuroinflammation. (C) 2016 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
WOS关键词EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ; NF-KAPPA-B ; (5R)-5-HYDROXYTRIPTOLIDE LLDT-8 ; MICROGLIA CELLS ; ACTIVATION ; LIPOPOLYSACCHARIDE ; ISCHEMIA ; BRAIN ; INHIBITION ; MECHANISMS
资助项目National Science Foundation of China[81571124] ; National Science Foundation of China[81371278] ; National Science Foundation of China[81373382] ; National Science Foundation of China[81471336] ; National Science Foundation of China[31300886] ; Specialized Research Fund for the Doctoral Program of Higher Education of China[20133201110017] ; Priority Academic Program Development of the Jiangsu Higher Education Institutes (PAPD)[00000000] ; Jiangsu key laboratory grant[BM2013003]
WOS研究方向Pharmacology & Pharmacy
语种英语
WOS记录号WOS:000379507700008
出版者JAPANESE PHARMACOLOGICAL SOC
源URL[http://119.78.100.183/handle/2S10ELR8/276012]  
专题药物化学研究室
通讯作者Cao, Ting; Jia, Jia
作者单位1.Soochow Univ, Coll Pharmaceut Sci, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China;
2.Chinese Acad Sci, Shanghai Inst Mat Med, 555 Rd Zu Chong Zhi,Zhangjiang Hi Tech Pk, Shanghai 201203, Peoples R China
3.Soochow Univ, Inst Neurosci, Suzhou 215123, Jiangsu, Peoples R China;
4.Soochow Univ, Jiangsu Key Lab Translat Res & Therapy Neuropsych, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China;
推荐引用方式
GB/T 7714		 Chen, Yanke,Zhang, Li,Ni, Jingshu,et al. LLDT-8 protects against cerebral ischemia/reperfusion injury by suppressing post-stroke inflammation[J]. JOURNAL OF PHARMACOLOGICAL SCIENCES,2016,131(2):131-137.
APA Chen, Yanke.,Zhang, Li.,Ni, Jingshu.,Wang, Xiaoyu.,Cheng, Jian.,...&Jia, Jia.(2016).LLDT-8 protects against cerebral ischemia/reperfusion injury by suppressing post-stroke inflammation.JOURNAL OF PHARMACOLOGICAL SCIENCES,131(2),131-137.
MLA Chen, Yanke,et al."LLDT-8 protects against cerebral ischemia/reperfusion injury by suppressing post-stroke inflammation".JOURNAL OF PHARMACOLOGICAL SCIENCES 131.2(2016):131-137.

入库方式： OAI收割

来源：上海药物研究所

浏览0
下载0
收藏0
其他版本

除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。