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The Effect of Ifn-Β Treatment on Plasma Levels of Bdnf and Il-6 in Relapsing-Remitting Multiple Sclerosis Patients Publisher Pubmed



Shajarian M1 ; Alsahebfosoul F2 ; Etemadifar M3
Authors
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Authors Affiliations
  1. 1. Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Department of Neurosurgery, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: NeuroImmunoModulation Published:2021


Abstract

Background: In recent investigations addressing neurodegenerative diseases, especially multiple sclerosis (MS), the roles of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) have been examined. Methods: Forty-five relapsing-remitting MS (RRMS) patients, including 32 IFN-β-treated and 13 newly identified untreated cases as well as 45 sex- and age-matched healthy controls, were recruited in the study. Plasma levels of BDNF and IL-6 were assessed using the ELISA method. Data were analyzed by SPSS (ver.21). Results: There were significant differences between the case and healthy control groups in terms of the plasma levels of BDNF (p value = 0.044) and IL-6 (p value <0.001). Besides, the treatment with IFN-β had no significant impact on the level of BDNF or IL-6 in RRMS patients as compared to healthy controls (p value = 0.716 and 0.623 for BDNF and IL-6, respectively). Furthermore, the increase in the plasma levels of BDNF and IL-6 indicated a direct correlation in the case group (r = 0.508, p value = 0.008). In detail, following the classification of the case group into 2 subgroups of IFN-β-treated and untreated patients, a direct positive correlation was observed between the plasma levels of BDNF and IL-6 in IFN-β-treated patients (r = 0.495, p value = 0.026). Conclusion: The IFN-β treatment seems not to be effective for upregulating BDNF and IL-6 in RRMS patients. © 2021 S. Karger AG, Basel. Copyright: All rights reserved.
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