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Effect of ulinastatin on the nerve regeneration of mice encephalomyelitis / 中国生化药物杂志
Article em Zh | WPRIM | ID: wpr-600299
Biblioteca responsável: WPRO
ABSTRACT
Objective To investigate the effects of ulinastatin(UTI)on the nerve regeneration of mice experimental allergic encephalomyelitis and the expression of related factors and protein.Methods Forty mice were randomly divided into four groups:ulinastatin group(U),atorvastatin group(A), empty control group(C)and normal control group(N).The experimental autoimmune encephalomyelitis(EAE)in mice was constructed by Freund's complete adjuvant and MOG35-55 polypeptide.Histopathological changes were observed by HE,LFB and Bielschowsky stained at the 3rd week and 4th week after immunized of each group.The expressions of CD4 +T cells were estimated by immunohistochemical method.The expression of myelin basic protein (MBP),brain-derived neurotrophic factor(BDNF),growth associated protein-43(GAP-43),2',3'-cyclic nucleotide-3'-phosphodiesterase(CNP)were detected by Western-blot.Results The largest neurological score of group U was lower than group C,and the difference was statistically significant(P<0.05 ).Pathological features showed that the inflammatory cells,demyelination of spinal cord and axonal injury of group U were lighter than group C.With the duration of treatment,nerve injury decreased.After UTI treatment,the expression of MBP,BDNF,GAP-43,CNP increased.They were statistically significant difference when compared with group C(P<0.05).There was no significant difference between ulinastatin and atorvastatin in the treatment of EAE.Conclusion Ulinastatin could reduce the extent of nerve damage effectively and promote its regeneration which provide a theoretical basis for the clinical treatment of MS.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Biochemical Pharmaceutics Ano de publicação: 2014 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Biochemical Pharmaceutics Ano de publicação: 2014 Tipo de documento: Article