Dariush Haghmorad1, Mohammad B Mahmoudi1, Mahmoud Mahmoudi2, Shahrzad Z T Rab1, Maryam Rastin1, Hamid Shegarfi3, Gholamreza Azizi4, Abbas Mirshafiey5. 1. Immunology Research Center, Buali Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran. 2. Genetics department, Shahid Sadoughi University of Medical Sciences, Yazd, Iran. 3. Institute for Surgical Research, Oslo University Hospital HF, Oslo, Norway. 4. Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran. 5. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran-14155, Box: 6446, Iran.
Abstract
OBJECTIVE: Multiple sclerosis (MS) is the most common inflammatory disease of the CNS. Experimental autoimmune encephalomyelitis (EAE) is a widely used model for MS. In the present research, our aim was to test the therapeutic efficacy of Calcium (Ca) in an experimental model of MS. METHODS: In this study the experiment was done on C57BL/6 mice. EAE was induced using 200 μg of the MOG35-55 peptide emulsified in CFA and injected subcutaneously on day 0 over two flank areas. In addition, 250 ng of pertussis toxin was injected on days 0 and 2. In the treatment group, 30 mg/kg Ca was administered intraperitoneally four times at regular 48 hour intervals. The mice were sacrificed 21 days after EAE induction and blood samples were taken from their hearts. The brains of mice were removed for histological analysis and their isolated splenocytes were cultured. RESULTS: Our results showed that treatment with Ca caused a significant reduction in the severity of the EAE. Histological analysis indicated that there was no plaque in brain sections of Ca treated group of mice whereas 4 ± 1 plaques were detected in brain sections of controls. The density of mononuclear infiltration in the CNS of Ca treated mice was lower than in controls. The serum level of Nitric Oxide in the treatment group was lower than in the control group but was not significant. Moreover, the levels of IFN-γ in cell culture supernatant of splenocytes in treated mice were significantly lower than in the control group. CONCLUSION: The data indicates that Ca intervention can effectively attenuate EAE progression.
OBJECTIVE:Multiple sclerosis (MS) is the most common inflammatory disease of the CNS. Experimental autoimmune encephalomyelitis (EAE) is a widely used model for MS. In the present research, our aim was to test the therapeutic efficacy of Calcium (Ca) in an experimental model of MS. METHODS: In this study the experiment was done on C57BL/6 mice. EAE was induced using 200 μg of the MOG35-55 peptide emulsified in CFA and injected subcutaneously on day 0 over two flank areas. In addition, 250 ng of pertussis toxin was injected on days 0 and 2. In the treatment group, 30 mg/kg Ca was administered intraperitoneally four times at regular 48 hour intervals. The mice were sacrificed 21 days after EAE induction and blood samples were taken from their hearts. The brains of mice were removed for histological analysis and their isolated splenocytes were cultured. RESULTS: Our results showed that treatment with Ca caused a significant reduction in the severity of the EAE. Histological analysis indicated that there was no plaque in brain sections of Ca treated group of mice whereas 4 ± 1 plaques were detected in brain sections of controls. The density of mononuclear infiltration in the CNS of Ca treated mice was lower than in controls. The serum level of Nitric Oxide in the treatment group was lower than in the control group but was not significant. Moreover, the levels of IFN-γ in cell culture supernatant of splenocytes in treated mice were significantly lower than in the control group. CONCLUSION: The data indicates that Ca intervention can effectively attenuate EAE progression.
Authors: Yanping Wang; Steven J Marling; Jinge G Zhu; Kyle S Severson; Hector F DeLuca Journal: Proc Natl Acad Sci U S A Date: 2012-05-16 Impact factor: 11.205
Authors: Lioba Horstmann; Heiko Schmid; André P Heinen; Florian C Kurschus; H Burkhard Dick; Stephanie C Joachim Journal: J Neuroinflammation Date: 2013-10-04 Impact factor: 8.322