Raw data related to: Coenzyme Q10 supplementation reduces peripheral oxidative stress and inflammation in interferon-β1a-treated multiple sclerosis

<p><strong>Abstract</strong></p> <p>Background: Oxidative stress is a driver of multiple sclerosis (MS) pathology. We evaluated&nbsp;the effect of coenzyme Q10 (CoQ10) on laboratory markers of oxidative stress and&nbsp;inflammation, and on MS clinical severity.</p> <p>Methods: We included 60 relapsing&ndash;remitting patients with MS treated with interferon beta1a&nbsp;44<strong>&mu;</strong>g (IFN-<strong>&beta;</strong>1a) with CoQ10 for 3 months, and with IFN-<strong>&beta;</strong>1a 44<strong>&mu;</strong>g alone for 3 more months (in&nbsp;an open-label crossover design). At baseline and at the 3 and 6-month visits, we measured&nbsp;markers of scavenging activity, oxidative damage and inflammation in the peripheral blood,&nbsp;and collected data on disease severity.</p> <p>Results: After 3 months, CoQ10 supplementation was associated with improved scavenging activity&nbsp;(as mediated by uric acid), reduced intracellular reactive oxygen species production, reduced&nbsp;oxidative DNA damage, and a shift towards a more anti-inflammatory milieu in the peripheral&nbsp;blood [with higher interleukin (IL)-4 and IL-13, and lower eotaxin, granulocyte-macrophage colonystimulating&nbsp;factor (GM-CSF), hepatocyte growth factor (HGF), interferon (IFN)-<strong>&gamma;</strong>, IL-1<strong>&alpha;</strong>, IL-2R,&nbsp;IL-9, IL-17F, macrophage inflammatory proteins (MIP)-1<strong>&alpha;</strong>, regulated on activation-normal T cell&nbsp;expressed and secreted (RANTES), tumor necrosis factor (TNF)-<strong>&alpha;</strong>, and vascular endothelial growth&nbsp;factor (VEGF). Also, CoQ10 supplementation was associated with lower Expanded Disability Status&nbsp;Scale, fatigue severity scale, Beck&rsquo;s depression inventory, and the visual analogue scale for pain.</p> <p>Conclusions: CoQ10 supplementation improved scavenging activity, reduced oxidative&nbsp;damage, and induced a shift towards a more anti-inflammatory milieu, in the peripheral blood&nbsp;of relapsing&ndash;remitting MS patients treated with 44<strong>&mu;</strong>g IFN-<strong>&beta;</strong>1a 44<strong>&mu;</strong>g. A possible clinical effect&nbsp;was noted but deserves to be confirmed over longer follow ups.</p> <p><strong>Progetto giovani ricercatori&nbsp;</strong>[GR-2016-02363725] dal titolo: &quot;Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression&quot;</p>