Vitamin D - an effective antioxidant in an animal model of progressive multiple sclerosis?
ECTRIMS Online Library. Hochmeister S. 279655; EP1513
Dr. Sonja Hochmeister
Dr. Sonja Hochmeister
Contributions
Abstract

Abstract: EP1513

Type:

Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms

M.T. Haindl1, M. Üçal2, W. Wonisch3, U. Schäfer2, M.Z. Adzemovic4, F. Fazekas1, S. Hochmeister1

1Neurology, 2Neurosurgery, 3Physiological Chemistry, Medical University of Graz, Graz, Austria, 4Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden

Vitamin D (vitD) is the most discussed antioxidant supplement for Multiple Sclerosis (MS) patients. Its functions include regulation of calcium homeostasis as well as effects on the immune response. Many studies already suggested correlations between a low vitD serum level and onset and progression of MS. At the same time, a positive effect of vitD on disease activity could be confirmed in well-established animal models of relapsing-remitting MS.
In our study we wanted to address whether vitD could have positive effects in progressive MS as well. For this purpose, we used our newly established rat model of cortical demyelination which covers most of the histopathological changes found in progressive MS (Ücal et al., 2017). One group of animals received 400 IE Vitamin D (Fresenius-Kabi, Graz, Austria) once weekly starting from weaning from their mothers at age 3 weeks (VitD-group, n = 5), the other group received standard rodent food only ('normal experimental conditions', NExC-group, n = 5).
As cortical pathology is most pronounced in our animal model on day 15 and myelin is partially restored again by day 30 we compared the extent of proteolipid protein (PLP) loss on immunohistochemical stainings at those dates between the NExC-group and VitD-group, respectively. Furthermore, we measured the total anti-oxidative capacity (TAC) and polyphenols (PP, attenuate oxidative stress) content in the serum of the rats via photometric tests.
We found significantly less PLP loss in the VitD-group (0.6±0.2 mm2 on day 15; 0.3±0.1 mm2 on day 30) compared to the NExC-group (0.9± 0.2 mm2 on day 15; 0.6±0.3 mm2 on day 30). Additionally only the VitD-group reached a high TAC level with 1.3±0.5 mmol/L on day 15 and 1.8±0.3 mmol/L on day 30 in comparison to the NExC-group where the TAC values stayed under the threshold of 1-1.3 mmol/L. The amount of protective PP was also higher in the VitD-group with 10±2 mM on day 15 and 12±0.5 mM on day 30 in comparison to the NExC-group with only 6±0.1 mM PP on day 15 and 8±0.5 mM PP on day 30.
In summary our preliminary data suggest a positive effect of vitD on cellular features of our progressive MS model possibly due to improved protection against reactive oxygen species. Further research including additional immunohistochemical analyses of different cell types and their quantitative evaluation as well as a greater number of cases concerning oxidative stress biomarkers are still required to complement these results.
Disclosure: This study was partially funded by Fresenius-Kabi (to Hochmeister S).
MTH declares no conflict of interest.
MÜ declares no conflict of interest.
WW declares no conflict of interest.
US declares no conflict of interest.
MZA declares no conflict of interest.
FF declares no conflict of interest.
SH declares no conflict of interest.

Abstract: EP1513

Type:

Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms

M.T. Haindl1, M. Üçal2, W. Wonisch3, U. Schäfer2, M.Z. Adzemovic4, F. Fazekas1, S. Hochmeister1

1Neurology, 2Neurosurgery, 3Physiological Chemistry, Medical University of Graz, Graz, Austria, 4Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden

Vitamin D (vitD) is the most discussed antioxidant supplement for Multiple Sclerosis (MS) patients. Its functions include regulation of calcium homeostasis as well as effects on the immune response. Many studies already suggested correlations between a low vitD serum level and onset and progression of MS. At the same time, a positive effect of vitD on disease activity could be confirmed in well-established animal models of relapsing-remitting MS.
In our study we wanted to address whether vitD could have positive effects in progressive MS as well. For this purpose, we used our newly established rat model of cortical demyelination which covers most of the histopathological changes found in progressive MS (Ücal et al., 2017). One group of animals received 400 IE Vitamin D (Fresenius-Kabi, Graz, Austria) once weekly starting from weaning from their mothers at age 3 weeks (VitD-group, n = 5), the other group received standard rodent food only ('normal experimental conditions', NExC-group, n = 5).
As cortical pathology is most pronounced in our animal model on day 15 and myelin is partially restored again by day 30 we compared the extent of proteolipid protein (PLP) loss on immunohistochemical stainings at those dates between the NExC-group and VitD-group, respectively. Furthermore, we measured the total anti-oxidative capacity (TAC) and polyphenols (PP, attenuate oxidative stress) content in the serum of the rats via photometric tests.
We found significantly less PLP loss in the VitD-group (0.6±0.2 mm2 on day 15; 0.3±0.1 mm2 on day 30) compared to the NExC-group (0.9± 0.2 mm2 on day 15; 0.6±0.3 mm2 on day 30). Additionally only the VitD-group reached a high TAC level with 1.3±0.5 mmol/L on day 15 and 1.8±0.3 mmol/L on day 30 in comparison to the NExC-group where the TAC values stayed under the threshold of 1-1.3 mmol/L. The amount of protective PP was also higher in the VitD-group with 10±2 mM on day 15 and 12±0.5 mM on day 30 in comparison to the NExC-group with only 6±0.1 mM PP on day 15 and 8±0.5 mM PP on day 30.
In summary our preliminary data suggest a positive effect of vitD on cellular features of our progressive MS model possibly due to improved protection against reactive oxygen species. Further research including additional immunohistochemical analyses of different cell types and their quantitative evaluation as well as a greater number of cases concerning oxidative stress biomarkers are still required to complement these results.
Disclosure: This study was partially funded by Fresenius-Kabi (to Hochmeister S).
MTH declares no conflict of interest.
MÜ declares no conflict of interest.
WW declares no conflict of interest.
US declares no conflict of interest.
MZA declares no conflict of interest.
FF declares no conflict of interest.
SH declares no conflict of interest.

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