Journal of Capital Medical University ›› 2012, Vol. 33 ›› Issue (3): 285-290.doi: 10.3969/j.issn.1006-7795.2012.03.001

• 中西医结合临床与基础 • Previous Articles     Next Articles

Study on repair of axonal damage and its mechanism in rats with experimental autoimmune encephalomyelitis induced by MBP68-86 and MBP87-99

ZHAO Hui1, WANG Yi-zhou2,3, KOU Shuang2, LI Ming2, QI Fang2, ZHANG Qiu-xia2, WANG Lei2   

  1. 1. Department of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Capital Medical University,Beijing 100069,China;2. Department of Chinese Materia Medica, School of Traditional Chinese Medicine, Capital Medical University,Beijing 100069,China;3. Medical Board of Concord Medical Services Holdings Limited,Beijing 100013,China
  • Received:2012-02-20 Revised:1900-01-01 Online:2012-06-21 Published:2012-06-21

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Abstract: Objective To observe the expression of amyloid precursor protein (APP) and growth-associated protein (GAP) -43 and the change of cyclic adenosine monophosphate (cAMP) /protein kinase (PKA) in rats with experimental autoimmune encephalomyelitis(EAE)induced by myelin basic protein (MBP)68-86 or MBP87-99, in order to explore the repair of axonal damage and its mechanism during the pathological process of EAE. Methods The rats were immunized by subcutaneous injection in both hind footpads with antigen containing MBP68-86 or MBP87-99, incomplete Freund's adjuvant (IFA) and mycobacterium tuberculosis. The neurological score and the pathological changes of brain tissues were observed, the cAMP was measured by ELISA and the mRNA expression of APP, GAP-43 and PKA in brain tissues was detected by real-time quantitative RT-PCR. Results Compared with the rats in MBP87-99 group, the progress of EAE was fast, the neurological scores were high, the inflammatory cell infiltration was severe, and even cuff-like change was found in MBP68-86 group. On the 14th day post-immunization (PI), the mRNA expression of GAP-43 in brain tissues of rats in medium-dose MBP68-86 group was down-regulated compared with normal group (P<0.05), the mRNA expression of APP was up-regulated on the 28th day PI (P<0.05). On the 28th day PI, the mRNA expression of APP was significantly increased in MBP87-99 group compared with normal group and low-dose MBP68-86 group (P<0.05), and the GAP-43 mRNA was also significantly increased compared with high and low-dose MBP68-86 group (P<0.05). On the 28th day PI, the cAMP level in brain tissues significantly increased in high and low-dose MBP68-86 group and MBP87-99 group compared with normal group (P<0.01or P<0.05), the PKA mRNA was also significantly increased in medium-dose MBP68-86 and MBP87-99 group (P<0.05 or P<0.01). Conclusion The EAE can be induced by both MBP68-86 and MBP87-99 in Lewis rats. It was caused by inflammatory cell infiltration, demyelination and axonal damage and other changes in the brain tissues, and it had a certain self-healing capability, which maybe related with the regulation on signaling pathway of cAMP-PKA. And it concluded that the rat EAE induced by middle-dose MBP68-86 was used for the experimental model in further study on the pathogenesis characteristics and medicine treatment.

Key words: experimental autoimmune encephalomyelitis, myelin basic protein, repair of axonal damage and its mechanism

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