期刊
JOURNAL OF NEUROIMMUNE PHARMACOLOGY
卷 4, 期 2, 页码 244-248出版社
SPRINGER
DOI: 10.1007/s11481-009-9147-5
关键词
astrocytes; CX3CL1; MAP kinase
资金
- United States Public Health Service [DA00924, DA025525]
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA025525] Funding Source: NIH RePORTER
CX3CL1 (fractalkine) has been shown not only to be neuroprotective but also may play a role in HIV-1-associated neuropathogenesis. In this study, we found that production of CX3CL1 by human astrocytes stimulated with interleukin (IL)-1 beta was inhibited in a concentration-dependent manner following pretreatment with the synthetic cannabinoid WIN55,212-2. The CB(2) receptor selective antagonist SR144528 significantly inhibited WIN55,212-2-mediated suppression of CX3CL1, suggesting a CB(2)-receptor-related mechanism. IL-1 beta triggered the activation of p38 and ERK1/2 (p44/42) MAP kinase (MAPK) signaling pathways, but WIN55,212-2 mainly inhibited p38 MAPK phosphorylation. This finding was mirrored in experiments using known inhibitors of these MAPKs, suggesting that the suppression of CX3CL1 production by WIN55,212-2 involves inhibition of signaling via p38 MAPK. Our results support the concept that synthetic cannabinoids have anti-inflammatory properties and that these agents may have therapeutic potential for certain neuroinflammatory disorders.
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