CoQ10: the new anti-inflammatory

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Relatively new discoveries in the research of inflammatory processes and diseases are the protein complexes  called inflammasomes. These are intracellular sensors of pathogenic damage, stress and metabolic danger, necessary for mediating host immune defences and maintaining cellular and intestinal integrity and homeostasis.[1]

Inflammasomes are critical for both innate and adaptive immune functions, with their activation triggering the maturation of the inflammatory cytokines interleukin (IL)-1 and IL-8.[1] However, if inflammasomes are overactive, or dysregulation occurs, they may contribute to persistent inflammation states and the onset of a wide range of diseases including inflammatory bowel disease (IBD), coeliac disease and type 1 diabetes.[2-4]

The most studied inflammasome is NRPL3, which is activated by a large number of triggers. Researchers postulate that the main triggers are reactive oxygen species (ROS) produced from factors such as damaged cells and mitochondria, pathogenic toxicity, environmental damage and dysbiosis.[1] This is where coenzyme Q10 (CoQ10) may play a crucial anti-inflammatory role. 

CoQ10 is a well-known antioxidant, active in every cell of the body. It has a strong link with cellular mitochondria, playing a role in oxidative processes and the electron transport chain (ETC). However, it may also have a crucial role in mitochondrial homeostasis and therefore down-regulation of NRPL3. 

In the gut, the NLRP3 protein is expresed in granulocytes, dendritic cells, monocytes, epithelial cells, T cells and B cells, with subcellular distribution localisation mainly in the cytoplasm.[1]

The activation of NRPL3 has been linked to mitochondrial ROS (mROS) production.[2] This may occur when mitochondria are ageing, dysfunctional, damaged, or with a metabolic overload causing increased permeability of the mitochondria membrane.[2,5] Dysfunctional mitochondria appear to be linked to numerous disease states. 

When excessive ROS production damages the mitochondria, mitophagy (mitochondrial autophagy or mitochondria destruction) occurs to dispose of the damaged organelles. If this process is dysfunctional, an accumulation of damaged mitochondria occurs, increasing ROS production. Likewise, when mitochondria lose membrane integrity due to a high ROS environment, cellular contents are released, which again increases the ROS load and may induce cell apoptosis.[6] Both of these processes trigger NRPL3 activation and the production of the inflammatory cytokines IL-1 and IL-8.

Additionally, as intestinal pathogens increase ROS production and inflammasome activation, dysbiosis may lead to mitochondrial membrane integrity issues and increased inflammation. However, dysbiosis may also occur due to mitochondrial dysfunction, with defects in mitophagy seen in Crohn’s disease or through inflammasome activation altering gut microbiota.[7,8]

Research utilising cell cultures have shown CoQ10 is capable of counteracting the triggers of inflammasome and maintaining mitochondrial homeostasis by:[5]

  • preventing mitochondrial dysfunction
  • inhibiting mitochondrial death
  • reducing ROS production
  • activating the gene expression for the growth and division of healthy mitochondria (a process called mitochondrial biogenesis). 

Additionally, in experimental colitis studies CoQ10 reduced the release of pro-inflammatory cytokines, promoted the expression of the anti-inflammatory cytokine IL-10 and preserved mitochondrial integrity.[6]

In recent research, fibromyalgia (FM), a condition commonly prescribed CoQ10, was studied in relation to inflammasome. Researchers found that subjects suffering from FM had mitochondrial respiratory chain dysfunction, increased mROS production and DNA oxidation, all activators of inflammasome, coupled with CoQ10 deficiency. Oral CoQ10 treatment showed a correlation between CoQ10 intake and decreased IL-1 and IL-8 and mROS levels, supporting the inhibitory effect of CoQ10 on inflammasome activation.[9]

References

  1. Ranson N, Eri R. The role of inflammasomes in intestinal inflammation. Am J Med Biolog Res 2013;1(3):64-76. [Full text]
     
  2. Harijith A, Ebenezer DL, Natarajan V. Reactive oxygen species at the crossroads of inflammasome and inflammation. Front Physiol 2014;5:352. [Full text]
     
  3. Zaki MH, Lamkanfi M, Kanneganti TD. The NLRP3 inflammasome: contributions to intestinal homeostasis. Trends Immunol 2011;32(4):171-179. [Full text]
     
  4. de Zoete MR, Palm NW, Zhu S, et al. Inflammasomes. Cold Spring Harb Perspect Biol 2014;6(12):a016287. [Full text]
     
  5. Jing L, He MT, Chang Y, et al. Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway. Int J Biol Sci 2015;11(1):59-66. [Full text]
     
  6. El Morsy EM, Kamel R, Ahmed MA. Attenuating effects of coenzyme Q10 and amlodipine in ulcerative colitis model in rats. Immunopharmacol Immunotoxicol 2015:1-8. [Abstract]
     
  7. Tschopp J. Mitochondria: sovereign of inflammation? Eur J Immunol 2011;41(5):1196-1202. [Abstract]
     
  8. Nicolson GL, Ash ME. Lipid replacement therapy: a natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Biochim Biophys Acta 2014;1838(6):1657-1679. [Full text]
     
  9. Cordero MD, Alcocer-Gomez E, Culic O, et al. NLRP3 inflammasome is activated in fibromyalgia: the effect of coenzyme Q10. Antioxid Redox Signal 2014;20(8):1169-1180. [Full text]

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Melissa_Peterson's picture
Melissa_Peterson

Melissa Peterson has been a writer and educator in the health and medical science fields for over 15 years. Naturopathically trained, Melissa also has postgraduate qualifications in literature research and reviewing. Her business, Words On Therapy, provides many services to industry including technical articles, white papers, blogs, SEO content, copywriting and research collation.