| Name | CoQ10 |
| Category | Anti-inflammatory |
Where to buy
 
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This is the Co-Q10 I take daily, I chose the ubiquinol form of Co-Q10 because studies show it has superior bioavailability. It seems to give my hair growth a huge boost, without it I can go for months without a haircut.
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CoQ10
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| Description |
Co Q-10 is an anti-oxidant and may promote growth and cell protection. It is normally found in the hundreds of mitochondria of each cell and is vital for the formation of Adenosine Triphoshate, the basic energy molecule used by each cell.
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| Typical Results |
N/A
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| Typical Dosages |
N/A
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| Significant Side Effects |
N/A
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| Pharmacology Pharmacodynamics |
N/A
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Clinical Studies
| Clinical Studies | Abstract |
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Coenzyme Q10: a novel gastroprotective effect via modulation of vascular permeability, prostaglandin E₂, nitric oxide and redox status in indomethacin-induced gastric ulcer model.
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Coenzyme Q10 is an essential cofactor in the mitochondrial electron transport pathway, and is endowed for its potent antioxidant capacity; characters that endorse its implication in several clinical practices and as a food supplement. Nevertheless, its potential gastro-protective effect, in acute models, has never been assessed, which is the objective of this study. Since indomethacin mediated gastropathy is multifaceted, including mitochondrial dysfunction and generation of reactive oxygen species, thus, the indomethacin-induced gastric injury serves as a convenient animal model for this work. Rats treated with indomethacin revealed mucosal hemorrhagic lesions, increased microvascular permeability and inhibited prostaglandin E₂ and mucus content. Redox imbalance was reflected by decreased mucosal glutathione (GSH), nitric oxide and glutathione peroxidase contents/activity, along with elevated lipid peroxides. Pretreatment with CoQ10 caused discernible decrease in indomethacin-induced gastric lesions, vascular permeability and lipid peroxide content. In addition, prostaglandin E₂ and GSH levels were restored, while those of nitric oxide and glutathione peroxidase were elevated significantly above normal; however, mucus formation was not altered significantly. The positive effects were comparable to those of sucralfate, the standard drug used herein, except for the mucus and prostaglandin E₂ levels that were increased above normal by sucralfate. CoQ10-mediated gastroprotective effect involves preservation of microvascular permeability, elevation of prostaglandin E₂, improvement of redox status, as well as boosting of nitric oxide. Nevertheless, maintaining gastric mucus content is ruled out.
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Anti-inflammatory effects of CoQ10 and colorless carotenoids.
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BACKGROUND:
CoQ10 (ubiquinone, coenzyme Q10) and carotenoids are popular antioxidants used in many skin care products to protect the skin from free radical damage.
AIM:
To evaluate the effects of CoQ10 and colorless carotenoids on the production of inflammatory mediators in human dermal fibroblasts treated with UV radiation (UVR) and to investigate the possible synergistic effects of these two antioxidants.
METHODS:
Normal human dermal fibroblast cell cultures were exposed to either 50 mJ of UVR or to IL-1 and then incubated with various concentrations of either CoQ10, the colorless carotenoids, phytoene and phytofluene, or to combinations of these antioxidants. After 24 h in culture, cells and spent medium were harvested and assayed by enzyme-linked immunosorbent assay for prostaglandin E2 (PGE-2), interleukin 6 (IL-6), and matrix metalloproteinase 1 (MMP-1). In addition, the ability of the carotenoids to protect CoQ10 from oxidation by the reactive oxygen species (ROS), hyperchlorite, was also determined.
RESULTS:
Human fibroblasts respond to UVR or to IL-1 by increasing the production of various inflammatory mediators including PGE-2, IL-1, and IL-6 and proteases such as collagenase (MMP-1). Treatment of fibroblasts with 10 microm of CoQ10 suppressed the UVR- or IL-1-induced increase in PGE-2, IL-6, and MMP-1. The combination of carotenoids and CoQ10 produced an enhanced inhibition of these three inflammatory mediators. Furthermore, the colorless carotenoids, phytoene and phytofluene, protected CoQ10 from degradation by the ROS, hypochlorite.
CONCLUSION:
CoQ10 is able to suppress the UVR- or IL-1-induced inflammatory response in dermal fibroblasts. Furthermore, this compound can block the UVR induction of the matrix-eroding enzyme, MMP-1. Finally, the combination of carotenoids plus CoQ10 results in enhanced suppression of inflammation. The results suggest that the combination of carotenoids and CoQ10 in topical skin care products may provide enhanced protection from inflammation and premature aging caused by sun exposure.
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