Study on the treatment of experimental autoimmune encephalomyelitis in rats by thymopentin
10.3760/cma.j.issn.0254-5101.2009.01.001
- VernacularTitle:胸腺五肽治疗实验性自身免疫性脑脊髓炎的实验研究
- Author:
Li GUO
;
Yu XU
;
Yifei ZHU
;
Xiuli WANG
;
Ying WANG
;
Bin LI
;
Yujie YUAN
;
Pingping ZHAO
;
Cuojun TAN
- Publication Type:Journal Article
- Keywords:
Experimental autoimmune encephalomyelitis;
Thymopentin;
IL-12;
IL-10
- From:
Chinese Journal of Microbiology and Immunology
2009;29(1):1-4
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the therapeutic effects of thymopentin(TP-5)for the experimentsl autoimmune encephalomyelitis(EAE)in rats.Metbods The EAE model wss established in wistar rats immunized with fresh guinea pig spinal cord homogenate(GPSCH)and complete Freund's adjuvant (CFA).Wistar rats were divided randomly into five groups:normal control group,EAE group,dexamethaSone(DXM)group,low dose TP-5 treated group,hish dose TP-5 treated group.The levels of IL-12 and IL-10 in serum of wistar rats were detected by sandwich-ELISA on day 7,14 and 21 post immunization.Resuits Morbidity and clinical score of low dose TP-5 treated group and DXM group were significantly lower than those of EAE group and hish dose TP-5 treated group(P＜0.01).Morbidity and clinical score of DXM group were significantly lower than those of low dose of TP-5 treated group(P＜0.01).The levels of IL-12 of EAE group,DXM group,low dose TP-5 treated group and high dose TP-5 treated group were significantly higher than of normal control group at each time point(P＜0.01).The levels of IL-12 of DXM group and low dose TP-5 treated group were significantly lower than that of EAE group(P＜0.01),meanwhile the levels of IL-10 of DXM group and low dose TP-5 treated group were significantly higher than that of the rest groups on day 14 and 21 post immunization(P＜0.01).Conclusion TP-5 has protective effects on EAE,and its functional mechanism may be associated with down.regulation of IL-12 as well as up-regulation of IL-10,so as to reverse the imbalance of TH1/TH2 responses by bidirectional regulation.
