Abstract OBJECTIVE: To study the pathological changes in the non-myelin sheath by observing histological damages to the neurofilament protein and apoptosis of neurons in rats with experimental autoimmune encephalomyelitis (EAE). METHODS: Forty-eight Wistar rats were randomly divided into two groups: control and EAE (24 rats in each group). Behavioral changes were observed. Inflammation reactions and demyelination were observed by hematoxylin eosin staining and LOYEZ staining.The level of neurofilament was detected by immunohistochemistry. Apoptosis of the neuron in the spinal cord was detected by TUNEL. RESULTS: Behavioral and histological results confirmed that the model of EAE rats was prepared successfully. In the EAE group, typical morphological features of axonal damage (sparsed axonal density, axonal distortion, axonal transection and even axonal disappearance) were found from the seventh day after immunization and the morphological changes were the most obvious on the fourteenth day. Neurofilament density in the EAE group was significantly lower than in the control group (P<0.01) at 7, 14 and 21 days after immunization. The neuronal apoptosis index in the EAE group at 7, 14 and 21 days after immunization was significantly higher than in the control group (P<0.01). CONCLUSIONS: In addition to inflammatory demyelination, axonal damage and neuronal apoptosis can be observed in the early stage of EAE. Pathological changes may be associated with neurological dysfunction.
ZHANG Jin-Feng,HUANG Rong,YANG Yu-Jia et al. Features of pathological changes in the non-myelin sheath of rats with experimental autoimmune encephalomyelitis[J]. 中国当代儿科杂志, 2012, 14(4): 306-309.
ZHANG Jin-Feng,HUANG Rong,YANG Yu-Jia et al. Features of pathological changes in the non-myelin sheath of rats with experimental autoimmune encephalomyelitis[J]. CJCP, 2012, 14(4): 306-309.
[1]Ercolini AM, Miller SD. Mechanisms of immunopathology in murine models of central nervous system demyelinating disease[J]. J Immunol, 2006, 176(6): 3293-3298.
[2]De Stefano N, Filippi M. MR spectroscopy in multiple sclerosis[J]. J Neuroimaging, 2007, 17(suppl 1): 31s-35s.
[3]Haghighi S, Andersen O, Odén A, Rosengren L. Cerebrospinal fluid markers in MS patient s and their healthy siblings[J]. Acta Neurol Scand, 2004, 109(2): 97-99.
[4]Lassmann H. Axonal and neuronal pathology in multiple sclerosis: what have we learnt from animal models[J]. Exp Neurol, 2010, 225(1): 2-8.
[5]Benson JM,Campbell KA,Guan Z, Gienapp IE, Stuckman SS, Forsthuber T, et al. T-cell activation and receptor downmodulation precede deletion induced by mucosally administered antigen[J]. J Clin Invest, 2000, 106(8): 1031-1038.
[6]Rovaris M, Gambini A, Gallo A, Falini A, Ghezzi A, Benedetti B, et al. Axonal injury in early multiple sclerosis is irreversible and independent of the shortterm disease evolution[J]. Neurology, 2005, 65(10): 1626-1630.
[7]Lee MA, Blamire AM, Pendlebury S, HO KH, Mills KR, Styles P, et al. Axonal injury or loss in the internal capsule and motor impairment in multiple sclerosis[J]. Arch Neurol, 2000, 57(1): 65-70.
[9]Linker RA, Sendtner M, Gold R. Mechanisms of axonal degeneration in EAE-lessons from CNTF and MHC I knockout mice[J]. J Neurol Sci, 2005, 233(1-2): 167-172.
[11]Wattjes MP, Harzheim M, Lutterbey GG,Klotz L, Schild HH, Tr-ber F. Axonal damage but no increased glial cell activity in the normal-appearing white matter of patients with clinically isolated syndromes suggestive of multiple sclerosis using high-field magnetic resonance spectroscopy[J]. AJNR Am J Neuroradiol, 2007, 28(8): 1517-1522.
[12]Niki'c I, Merkler D, Sorbara C, Brinkoetter M, Kreutzfeldt M, Bareyre FM, et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis[J]. Nat Med, 2011, 17(4): 495-499.