期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 109, 期 2, 页码 105-111出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0165-5728(00)00279-4
关键词
experimental autoimmune encephalomyelitis; multiple sclerosis; tumor necrosis factor; interleukin-6; peripheral-type benzodiazepine receptor; pentraxin 3; PK11195; dexamethasone; rolipram
We have studied the mRNA expression of pentraxin 3 (PTX3) and the binding of the peripheral-type benzodiazepine receptor (PBR) ligand, [H-3]-PK11195, in the spinal cord of Lewis rats where EAE was actively induced. PTX3 was induced during the active phase of EAE (day 10-14), it remained high up to 30 days and disappeared only 60 days later. Similarly, PK11195 binding peaked at day 14-17 during the recovery and it disappeared by day 60. On the other hand, the levels of TNF and LL-S in the spinal cord were elevated at the peak and at the onset of clinical signs and returned to non-detectable by day 14-17. Dexamethasone abolished all these changes, while treatment with rolipram, delayed the appearance of the disease and then decreased its severity. However the peaks of TNF, IL-6, PER and PTX3 levels in spinal cord were only delayed, but not reduced, by rolipram treatment. In conclusion, we show two types of inflammatory changes in EAE: acute, short term changes (TNF and IL-6), that correlate with the disease; and effects such as PTX3 expression and PK11195 binding that last longer after recovery from the disease. (C) 2000 Elsevier Science B.V. All rights reserved.
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