Naddafi Fatemeh, Reza Haidari Mohsen, Azizi Gholamreza, Sedaghat Reza, Mirshafiey Abbas
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.
Innov Clin Neurosci. 2013 Apr;10(4):20-5.
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.
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.
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.
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.
多发性硬化症是一种中枢神经系统的自身免疫性神经退行性疾病。多发性硬化症的病因仍不清楚，且尚无治愈方法。实验性自身免疫性脑脊髓炎被认为是多发性硬化症的动物模型。尼古丁的治疗作用已被证明在阿尔茨海默病和帕金森病中均有效，因此我们首次研究了尼古丁在实验性自身免疫性脑脊髓炎模型中的作用。
根据张广献等人的方法诱导实验性自身免疫性脑脊髓炎。在免疫后第7天开始用尼古丁治疗。在免疫前第7天开始用尼古丁预防。此外，为了进行体外分析，我们使用U-87 MG细胞系，分别通过MTT、ELISA和酶谱分析方法评估尼古丁对细胞增殖抑制作用、促炎细胞因子（TNF-α、IL-1β、IL-6）和MMP-2活性的影响。此外，取出小鼠的大脑进行组织学分析。
我们的研究结果表明，用尼古丁治疗可显著降低实验性自身免疫性脑脊髓炎的严重程度和发病时间。组织学分析表明，尼古丁预防组和治疗组的脑切片中分别有非常轻微和轻微的斑块。
我们的数据表明，尼古丁可显著改善临床评分，并减轻实验性自身免疫性脑脊髓炎中典型的脱髓鞘病理，表明尼古丁在多发性硬化症实验模型中具有保护作用。
