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. 2019 Feb 18:12:1756286418819074.
doi: 10.1177/1756286418819074. eCollection 2019.

Coenzyme Q10 supplementation reduces peripheral oxidative stress and inflammation in interferon-β1a-treated multiple sclerosis

Affiliations

Coenzyme Q10 supplementation reduces peripheral oxidative stress and inflammation in interferon-β1a-treated multiple sclerosis

Marcello Moccia et al. Ther Adv Neurol Disord. .

Abstract

Background: Oxidative stress is a driver of multiple sclerosis (MS) pathology. We evaluated the effect of coenzyme Q10 (CoQ10) on laboratory markers of oxidative stress and inflammation, and on MS clinical severity.

Methods: We included 60 relapsing-remitting patients with MS treated with interferon beta1a 44μg (IFN-β1a) with CoQ10 for 3 months, and with IFN-β1a 44μg alone for 3 more months (in an open-label crossover design). At baseline and at the 3 and 6-month visits, we measured markers of scavenging activity, oxidative damage and inflammation in the peripheral blood, and collected data on disease severity.

Results: After 3 months, CoQ10 supplementation was associated with improved scavenging activity (as mediated by uric acid), reduced intracellular reactive oxygen species production, reduced oxidative DNA damage, and a shift towards a more anti-inflammatory milieu in the peripheral blood [with higher interleukin (IL)-4 and IL-13, and lower eotaxin, granulocyte-macrophage colony-stimulating factor (GM-CSF), hepatocyte growth factor (HGF), interferon (IFN)-γ, IL-1α, IL-2R, IL-9, IL-17F, macrophage inflammatory proteins (MIP)-1α, regulated on activation-normal T cell expressed and secreted (RANTES), tumor necrosis factor (TNF)-α, and vascular endothelial growth factor (VEGF). Also, CoQ10 supplementation was associated with lower Expanded Disability Status Scale, fatigue severity scale, Beck's depression inventory, and the visual analogue scale for pain.

Conclusions: CoQ10 supplementation improved scavenging activity, reduced oxidative damage, and induced a shift towards a more anti-inflammatory milieu, in the peripheral blood of relapsing-remitting MS patients treated with 44μg IFN-β1a 44μg. A possible clinical effect was noted but deserves to be confirmed over longer follow ups.

Keywords: antioxidant; coenzyme Q10; inflammation; multiple sclerosis; oxidative stress.

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Conflict of interest statement

Conflict of interest statement: MM received research grants from MAGNIMS-ECTRIMS and Merck. GM received research grants from Merck, Biogen Idec and Novartis. VBM and RL received honoraria from Almirall, Bayer, Biogen Idec, Genzyme, Merck, Novartis, and Roche.

Figures

Figure 1.
Figure 1.
Study design. A crossover design was considered. Group1 received CoQ10 supplementation along with IFN-β1a over the first 3 months, followed by IFN-β1a alone for 3 months; Group 2 received IFN-β1a alone over the first 3 months, followed by CoQ10 supplementation along with IFN-β1a for 3 months. CoQ10, coenzyme Q10; IFN-β1a, interferon-beta1a.
Figure 2.
Figure 2.
Laboratory outcomes. Profile plots show variations of laboratory outcomes over time in relation to the use of IFN-β1a alone or in combination with Coenzyme Q10 (Group 1: group receiving Coenzyme Q10 from baseline to 3-month follow up is in red; Group 2: group receiving Coenzyme Q10 from 3- to 6-month follow up is in green). Coefficients (Coeff) and p values are shown from mixed-effect linear regression models where an interaction term between treatment and time was set and marginal effects were calculated. IFN-β1a, interferon-beta1a.
Figure 3.
Figure 3.
Clinical outcomes. Profile plots show variations of clinical outcomes over time in relation to the use of IFN-β1a alone or in combination with Coenzyme Q10 (Group 1: group receiving Coenzyme Q10 from baseline to 3-month follow up is in red; Group 2: group receiving Coenzyme Q10 from 3- to 6-month follow up is in green). Coefficients (Coeff) and p values are shown from mixed-effect linear regression models where an interaction term between treatment and time was set and marginal effects were calculated. IFN-β1a, interferon-beta1a.

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