Expression of NgR in experimental allergic encephalomyelitis (EAE) and intervention of NgR (310)ecto-Fc in EAE
10.3760/cma.j.issn.1671-8925.2010.11.002
- VernacularTitle:NgR在实验性自身免疫性脑脊髓炎中的表达及NgR(310)ecto-Fc的干预作用
- Author:
Cong GAO
1
;
Ting-Ting ZHAN
;
Fu-Hua XIE
;
Mei-Rong LIN
;
Ze-Cong LIN
Author Information
1. 广州医学院附属第二医院
- Keywords:
Experimental allergic encephalomyelitis;
NgR(310)ecto-Fc;
Nogo-66(NgR)
- From:
Chinese Journal of Neuromedicine
2010;09(11):1086-1089
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role and the mechanism of NgR (310)ecto-Fc in experimental allergic encephalomyelitis (EAE). Methods EAE models were successfully induced in 90 Lewis rats and equally randomized into group A (without treatment), group B (giving NgR(310)ecto-Fc treatment 1 d after the success of model making) and group C (giving NgR(310)ecto-Fc treatment right after onset of the disease). The clinical scores, pathological changes of the animals were observed and compared before and after treatment. Changes of NgR expression and counts of NgR(310)ecto-Fc positive cells in the myeloid tissue were tested by immunohistochemistry before and after treatment.Results Clinical scores in group B (3.020±1.017, 1.365±0.127) and group C (2.853±0.958, 1.275±0.092) were significantly lower than those in group A (4.476± 1.525, 1.894+0.135) on the 15th and 25th d of success of model making (P＜0.05), while no significant differences on the clinical scores were noted between group B and group C. NgR expression was observed in the myeloid tissue of all groups; the counts of NgR(310)ecto-Fc positive cells in the myeloid tissue in group B (79.07± 10.31, 45.89±4.77) and group C (70.47±7.40, 40.63±4.15) were obviously decreased as compared with those in group A (101.12±11.97, 62.95±7.11) on the 15th and 25th d of success of model making (P＜0.05); while no significant differences on the counts of NgR (310)ecto-Fc positive cells were noted between group B and group C (P＞0.05). Conclusion NgR (310)ecto-Fc can alleviate the clinical symptoms of EAE by suppressing the expression of NgR, leading to no activation of myelin-related inhibitory factor (Nogo-A, MAG and OMgp), and inducing the growth of axons in EAE.
