The neuroprotective effect of ulinastatin in mice with experimental autoimmune encephalomyelitis
10.3760/cma.j.issn.1006-7876.2011.07.007
- VernacularTitle:乌司他丁对实验性自身免疫性脑脊髓炎小鼠神经的保护作用
- Author:
Yaqing SHU
;
Yu YANG
;
Xueqiang HU
;
Ying LI
;
Ming FENG
- Publication Type:Journal Article
- Keywords:
Glycoproteins;
Encephalomyelitis,autoimmune,experimental;
Brain-derived neurotrophic factor;
Nerve regeneration
- From:
Chinese Journal of Neurology
2011;44(7):464-467
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of ulinastatin (UTI) on the expression of brainderived neurotrophic factor ( BDNF ) and remyelination in mice with experimental autoimmune encephalomyelitis ( EAE).Methods Twenty-four C57BL/6 mice were randomly divided into UTI group (U),normal saline treated group (S) and normal control group (N,n = 8,respectively).Demyelinations in the spinal cord were observed by solochrome cyanin staining.The expression of BDNF,myelin basic protein (MBP),and 2',3 '-cyclic nucleotide 3'-phosphodiesterase (CNP) in brain tissue of each group were evaluated by Western blot.Results Average clinical scores in group U at the 12,13,14,22,23,31,33,34 and 35 days were 0,0.25,0.38,0.63,0.63,0.40,0.40,0.40 and 0.40 respectively.They were significantly lower than group S at the same time ( U= 16.00,15.00,14.50,7.50,0.00,14.50,14.50,12.00 and 14.50,all P ＜0.05).Solochrome cyanin staining showed that demyelination of spinal cord in group U was also significantly improved than group S.Expressions of BDNF ( 1.96 ± 0.29),MBP (2.67 ± 0.48 ) and CNP ( 1.75 ± 0.20) in group U were all significantly higher than group S ( There were 0.80 ± 0.15,1.36 ± 0.38 and 1.06 ± 0.18 respectively,all P ＜ 0.05).Conclusions UTI has protective effect on EAE.The possible mechanism is that it could promote remyelination,and protect oligodendrocytes and neurons in EAE model by increasing BDNF expression in brain.
