期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 221, 期 1-2, 页码 46-52出版社
ELSEVIER
DOI: 10.1016/j.jneuroim.2010.02.011
关键词
Inflammation; Complement system; Anaphylatoxins; Brain; Systemic lupus erythematosus
资金
- National Institutes of Health [R01DK055357]
- American Heart Association [0855717G]
To investigate the role of C5a generated on complement activation in brain, the lupus model, MRL/lpr mice were treated with C5a receptor(R) antagonist (ant). Neutrophil infiltration, ICAM, TNF-alpha and iNOS mRNA expression, neuronal apoptosis and the expression of p-JNK, pSTAT1 and p-Erk were reduced and p-Akt increased on C5aR inhibition in MRL/lpr brains. MRL/lpr serum caused increased apoptosis in neurons showing that lupus had a direct effect on these cells. C5aRant pretreatment prevented the lupus serum induced loss of neuronal cells. Our findings demonstrate for the first time that C5a/C5aR signaling plays an important role in the pathogenesis of CNS lupus. (C) 2010 Published by Elsevier B.V.
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