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CoQ10 Reduces Inflammasome Activation in Fibromyalgia Patients

  [ 6 votes ]   [ Discuss This Article ]
www.ProHealth.com • July 28, 2013


Editor's comment: Inflammasomes are multiprotein molecular complexes that sense a wide variety of pathogens and are key players in the inflammatory response.  While inflammasomes are part of an important immune response that can protect the body, when there is overwhelming damage or infection, the ensuing inflammatory response can become chronic and injurious to the body.  This type of response can be seen in a number of autoinflammatory and autoimmune disorders.     

Other studies have demonstrated that mitochondrial dysfunction triggers activation of the NLRP3 inflammasome.  This study found that treating fibromyalgia patients with CoQ10, which is known to support mitochondrial function, also reduced  NLRP3 inflammasome activation. 


NLRP3 Inflammasome is activated in Fibromyalgia: the effect of Coenzyme Q10.

By Mario D. Cordero, et al.

Abstract:

Aims: Fibromyalgia (FM) is a prevalent chronic pain syndrome characterized by generalized hyperalgesia associated with a wide spectrum of symptoms such as fatigue and joint stiffness. Diagnosis of FM is difficult due to the lack of reliable diagnostic biomarkers, while treatment is largely inadequate.

We have investigated the role of coenzyme Q10 (CoQ10) deficiency and mitochondrial dysfunction in inflammasome activation in blood cells from FM patients, and in vitro and in vivo CoQ10 deficiency models.

Results:

  • Mitochondrial dysfunction was accompanied by increased protein expression of IL-1β, NLRP3 and caspase-1 activation, and increase of serum levels of pro-inflammatory cytokines (IL-1β and IL-18).

  • CoQ10 deficiency induced by p-aminobenzoate treatment in BMCs and mice showed NLRP3 inflammasome activation with marked algesia.

  • A placebo-controlled trial of CoQ10 in FM patients has shown a reduced NLRP3 inflammasome activation and IL-1β and IL-18 serum levels.

Innovations: These results show an important role for the NLRP3 inflammasome in the pathogenesis of FM, and the capacity of CoQ10 in the control of inflammasome.

Conclusions: These findings provide new insights into the pathogenesis of FM and suggest that NLRP3 inflammasome inhibition represents a new therapeutic intervention for the disease.

Source: Antioxidant & Redox Signaling, July 25, 2013. By Mario D. Cordero, Elisabet Alcocer-Gómez, Ognjen Culic, Angel M. Carrión, Manuel de Miguel, Eduardo Díaz-Parrado, Eva M. Perez-Villegas, Pedro Bullon, Maurizio Battino and José A. Sánchez-Alcázar.  Dpto. Citología e Histología Normal y Patológica, Facultad de Medicina. Universidad de Sevilla, 41009 Sevilla-Spain, Avda. Sánchez-Pizjuán s/n , Sevilla, Spain, 41009.




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