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Báo cáo khoa học: "Melatonin ameliorates autoimmune encephalomyelitis through suppression of intercellular adhesion molecule-1"

Tuyển tập các báo cáo nghiên cứu khoa học quốc tế về bệnh thú y đề tài: Melatonin ameliorates autoimmune encephalomyelitis through suppression of intercellular adhesion molecule-1 | J. Vet. Sci. 2001 2 2 85-89 OURNAL OF Veterinary Science Melatonin ameliorates autoimmune encephalomyelitis through suppression of intercellular adhesion molecule-1 JongChul Kang Meejung Ahn Yong-Sik Kim1 Changjong Moon Yongduk Lee Myung-Bok Wie Young-jae Lee and Taekyun Shin Department of Veterinary Medicine Institute for Life Science BK21 Cheju National University Cheju 690-756 Korea 1 Department of Pharmacology College of Medicine Seoul National University Seoul 110-799 Korea Melatonin N-acetyl-5-methoxytryptamine a pineal neurohormone is a hydroxyl radical scavenger and antioxidant and plays an important role in the immune system. We studied the effect of exogenous melatonin on the pathogenesis of experimental autoimmune encephalomyelitis EAE . EAE was induced in Lewis rats by immunization with rat spinal cord homogenates. Subsequent oral administration of melatonin at 5 mg kg significantly reduced the clinical severity of EAE paralysis compared with administration of the vehicle alone p 0.01 . Infiltration of ED1 macrophages and CD4 T cells into spinal cords occurred both in the absence and presence of melatonin treatment but melatonin-treated rats had less spinal cord infiltration of inflammatory cells than did the control group. ICAM-1 immunoreactivity in the blood vessels of EAE lesions was decreased in melatonin-treated rats compared to vehicle-treated rats. These findings suggest that exogenous melatonin ameliorates EAE via a mechanism involving reduced expression of ICAM-1 and lymphocyte function-associated antigen-1a in autoimmune target organs. Key words Melatonin experimental autoimmune encephalomyelitis intercellular adhesion molecule-1 Introduction Experimental autoimmune encephalomyelitis EAE is an autoimmune disease of the central nervous system CNS that is a model for human demyelinating diseases such as multiple sclerosis 24 . The clinical course of EAE is characterized by weight loss ascending paralysis and spontaneous recovery. EAE is .