Fatemeh Naddafi1, Mohsen Reza Haidari, Gholamreza Azizi, Reza Sedaghat, Abbas Mirshafiey. 1. Ms. Naddafi is from Department of Cellular and Molecular Biology, Kish International Campus, University of Tehran, Tehran, Iran; Dr. Haidari is from Department of Neurology, Faculty of Medicine, Baqiyatallah University of Medical Sciences, Tehran, Iran; Mr. Azizi is from Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Kara], Iran; Dr. Sedaghat is from Department of Anatomy and Pathology, Faculty of Medicine, Shahed University, Tehran, Iran; and Dr. Mirshafiey is from Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Abstract
BACKGROUND: Multiple sclerosis is an autoimmune, neurodegenerative disease of the central nervous system. The cause of multiple sclerosis is still unknown, and there is no cure for multiple sclerosis. Experimental autoimmune encephalomyelitis is considered as an animal model for multiple sclerosis. The therapeutic role of nicotine has been proven to be effective in both Alzheimer's and Parkinson's disease, thus we examined, for the first time, the role of nicotine in the experimental autoimmune encephalomyelitis model. METHODS: Experimental autoimmune encephalomyelitis induction was performed according to Guang-Xian Zhang et al. Treatment with nicotine was started on Day 7 post-immunization. Prevention with nicotine was started on Day 7 pre-immunization. Also for in-vitro analysis, we used U-87 MG cell line to evaluate the inhibitory effect of nicotine in cell proliferation, pro-inflammatory cytokines (TNF-alpha, IL-lbeta, IL-6) and MMP-2 activity by MTT, ELISA, and zymoanalysis methods, respectively. Moreover, the brains of mice were removed for histological analysis. RESULTS: Our findings showed that treatment with nicotine caused a significant reduction in the severity and onset of the experimental autoimmune encephalomyelitis. Histological analysis indicated that there was very mild and mild plaque in the brain sections of nicotine prevention and treatment groups, respectively. CONCLUSION: Our data indicate that nicotine can significantly improve the clinical score and attenuate the demyelinating pathology typically found in experimental autoimmune encephalomyelitis, indicating that nicotine has protective effects in experimental model of multiple sclerosis.
BACKGROUND:Multiple sclerosis is an autoimmune, neurodegenerative disease of the central nervous system. The cause of multiple sclerosis is still unknown, and there is no cure for multiple sclerosis. Experimental autoimmune encephalomyelitis is considered as an animal model for multiple sclerosis. The therapeutic role of nicotine has been proven to be effective in both Alzheimer's and Parkinson's disease, thus we examined, for the first time, the role of nicotine in the experimental autoimmune encephalomyelitis model. METHODS: Experimental autoimmune encephalomyelitis induction was performed according to Guang-Xian Zhang et al. Treatment with nicotine was started on Day 7 post-immunization. Prevention with nicotine was started on Day 7 pre-immunization. Also for in-vitro analysis, we used U-87 MG cell line to evaluate the inhibitory effect of nicotine in cell proliferation, pro-inflammatory cytokines (TNF-alpha, IL-lbeta, IL-6) and MMP-2 activity by MTT, ELISA, and zymoanalysis methods, respectively. Moreover, the brains of mice were removed for histological analysis. RESULTS: Our findings showed that treatment with nicotine caused a significant reduction in the severity and onset of the experimental autoimmune encephalomyelitis. Histological analysis indicated that there was very mild and mild plaque in the brain sections of nicotine prevention and treatment groups, respectively. CONCLUSION: Our data indicate that nicotine can significantly improve the clinical score and attenuate the demyelinating pathology typically found in experimental autoimmune encephalomyelitis, indicating that nicotine has protective effects in experimental model of multiple sclerosis.
Authors: Paresh Thakker; Michael W Leach; Wen Kuang; Stephen E Benoit; John P Leonard; Suzana Marusic Journal: J Immunol Date: 2007-02-15 Impact factor: 5.422