Anti-Aging Compound Myricetin offers Heart, Brain, and Anti-Cancer Benefits

Myricetin is a naturally-occurring phenolic compound that is found in vegetables, fruits, nuts, berries, tea, and red wine. “Myricetin is a common plant-derived flavonoid and is well recognized for its nutraceuticals value,” D. K. Semwal and colleagues at South Africa’s Tshwane University of Technology remark in a recent review.

The compound exhibits a wide range of activities that include strong antioxidant, anticancer, antidiabetic and anti-inflammatory activities. It displays several activities that are beneficial for the central nervous system and numerous studies have suggested that the compound may be beneficial to protect against diseases such as Parkinson's and Alzheimer's.”1 In an evaluation of compounds derived from the plant Triclisia gilletii, myricetin showed activity against a resistant strain of Mycobacterium tuberculosis.2 In another study, myricetin and glycosylated metabolites of myricetin inhibited human immunodeficiency virus (HIV) type 1.3

Cardiovascular Research on Myricetin

An investigation of eight plant compounds found that myricetin protected human vascular endothelial cells from hydrogen peroxide-induced oxidative injury and lowered the formation of thiobarbituric acid reactive substances (TBARS, a marker of lipid peroxidation).4 “Taken all together the results indicate myricetin as the most active agent among the selected plant-derived polyhydroxyl compounds, with prominent capacities against oxidized LDL and reactive oxygen species production in human umbilical vascular endothelial cells,” R. Bertin and colleagues conclude.

In the heart, myricetin reduced the ability of the proinflammatory compound lipopolysaccharide to cause injury in a mouse model of sepsis-induced myocardial dysfunction.5 The compound decreased the production of inflammatory cytokines in heart tissue and serum while reducing apoptosis (programmed cell death), thereby preventing the impairment in cardiac function that was observed in animals that did not receive myricetin.

In experiments involving skin cells known as keratinocytes, and also fibroblasts and endothelial cells, myricetin-3-O-beta-rhamnoside and the phenolic compound chlorogenic acid exhibited wound healing properties.6 Myricetin has also been found to protect against ultraviolet-B damage in human keratinocytes.7

Research in mice in which diabetes was induced by the administration of streptozotocin revealed that six months of treatment with myricetin reduced cardiac hypertrophy, apoptosis, and interstitial fibrosis.8 Myricetin was found to strengthen antioxidative activity and decrease the production of malondialdehyde, a marker of oxidative stress, while lowering the secretion of the inflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha. The authors concluded that myricetin possesses potential protective effects against diabetic cardiomyopathy, which is associated with an increased risk of premature mortality in diabetics.

Myricetin, Brain, and Cognitive Function

Research has revealed that myricetin can reduce some of the consequences of the genetic abnormalities in Huntington’s disease while improving neurobehavioral deficits in a mouse model.9 The research suggests that myricetin could be investigated as a treatment for Huntington’s disease and related disorders.

In a mouse model of Alzheimer’s disease, myricetin reversed cognitive deficits by inhibiting acetylcholinesterase (the enzyme that breaks down the neurotransmitter acetylcholine), and by downregulating brain iron.10 Myricetin lowered oxidative damage and increased antioxidant enzyme activity, an effect that was prevented by a high iron diet.

In a study involving mice in which cognitive impairment was induced by the administration of D-galactose, myricetin significantly improved memory and learning.11 Myricetin has demonstrated the ability to protect against glutamate-induced excitotoxicity, and the authors concluded that “myricetin is a potent antineurodegenerative compound and may contribute to the discovery of a drug with which to combat neurodegeneration.”12

Myricetin and Cancer

A review of natural compounds used in the treatment of non-small cell lung cancer included information concerning the benefit of myricetin.13 “Myricetin, a flavonoid commonly found in tea, wines, berries, fruits, and medicinal plants, has been reported to possess antioxidative, antiproliferative, and anti-inflammatory qualities,” Chih-Yang Huang and colleagues write. “Previous studies have shown that myricetin exerts an antiproliferative effect on lung, esophageal, leukemia, and prostate cancer cells. Myricetin may act as a direct antioxidant that scavenges or quenches oxygen free radicals, and as an indirect antioxidant that induces antioxidant enzymes to protect cells against hydrogen peroxide-induced cell damage.”

Myricetin’s anti-inflammatory effect showed an ability to prevent chronic inflammation and decreased the size of colon polyps, a precursor of colorectal cancer in mice.14 The compound lowered levels of the inflammatory factors interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, nuclear factor NF-κB, cyclooxygenase-2 (COX-2), and other factors in colon tissues. The findings suggest its use “as a promising chemopreventive drug for reducing the risk of colorectal cancer”, according to authors M. J. Zhang and colleagues.

In oral squamous cell carcinoma cells, myricetin impaired cell cycle progression and inhibited metastasis.15 In placental choriocarcinoma (a cancer that affects pregnant women) cells, myricetin decreased cell proliferation and promoted apoptosis.16 It also showed synergistic effects with the chemotherapies etoposide and cisplatin. In anaplastic thyroid cancer (an often lethal form of thyroid cancer) cells, myricetin reduced proliferation by about 70%.17 In human glioma (a cancer of the brain and spinal cord) cells, myricetin inhibited cell migration, induced apoptosis and elicited other anticancer effects.18 The compound has shown an ability to induce apoptosis and other effects in human ovarian, esophageal, colon, prostate, bladder, pancreatic, liver, and stomach cancer cells.19-26

Myricetin has additionally shown an ability to enhance natural killer cell activity, which can increase the ability to combat cancer.27

“An increasing number of studies have shown the beneficial effects of myricetin against different types of cancer by modifying several cancer hallmarks including aberrant cell proliferation, signaling pathways, apoptosis, angiogenesis, and tumor metastasis,” writes K. P. Devi and colleagues in a 2015 review. “Most importantly, myricetin interacts with oncoproteins such as protein kinase B (PKB) (Akt), Fyn, MEK1, and JAK1-STAT3 (Janus kinase-signal transducer and activator of transcription 3), and it attenuates the neoplastic transformation of cancer cells. In addition, myricetin exerts antimitotic effects by targeting the overexpression of cyclin-dependent kinase 1 (CDK1) in liver cancer.”28

Lifespan and Anti-aging Effects

In regard to myricetin’s potential benefits, here's the best part: research has found that the compound extended average lifespan by 32.9% when administered to the roundworm Caenorhabditis elegans.29 Longer life was accompanied by a decline in reactive oxygen species accumulation and less formation of lipofuscin which is “a pigment consisting of highly oxidized and cross-linked proteins that is considered as a biomarker of aging in diverse species.” However, the authors conclude that, rather than its direct antioxidant effects, myricetin’s lifespan-extending benefit is dependent on the transcription factors DAF-16.

On the research horizon, the structure of myricetin helped in the development of a new compound (Proxison) that has even greater antioxidant potency.30 “This novel antioxidant can be applied to investigate oxidative stress in disease models, like alpha-synucleinopathies and other neurodegeneration models,” Nicola J. Drummond and colleagues conclude. “In addition, Proxison could have applications for regenerative medicine where oxidative stress has been implicated in poor cell survival of transplanted cells, with the advantage that the molecule can be pre-loaded into cells prior to transplantation. Proxison could also have applications for conditions, such as stroke or cardiac infarction, in which a temporary, but acute, exposure to oxidative stress is experienced, as well as diseases in which oxidative stress and mitochondrial dysfunction are core features.”

Furthermore, myricetin was recently identified as one of a handful of compounds that modify senescence-inducing pathways.31 This and other research suggests its use by humans to help decelerate aging. It will be of benefit to all life extensionists to keep up-to-date concerning the outcome of future research involving this promising flavonoid.

References

  1. Semwal DK et al. Nutrients. 2016 Feb 16;8(2):90.
  2. Tiam ER et al. Nat Prod Res. 2017 Nov 16:1-9.
  3. Ortega JT et al. AIDS Res Ther. 2017 Oct 12;14(1):57.
  4. Bertin R et al. Biomed Pharmacother. 2016 Aug;82:472-8.
  5. Zhang N et al. Phytother Res. 2017 Dec 7.
  6. Moghadam SE et al. Molecules. 2017 Sep 8;22(9).
  7. Huang JH et al. Toxicol In Vitro. 2010 Feb;24(1):21-8.
  8. Liao HH et al. Oxid Med Cell Longev. 2017;2017:8370593.
  9. Khan E et al. ACS Chem Biol. 2017 Nov 27.
  10. Wang B et al. Biochem Biophys Res Commun. 2017 Aug 19;490(2):336-342.
  11. Lei Y et al. Food Chem. 2012 Dec 15;135(4):2702-7.
  12. Shimmyo Y et al. J Neurosci Res. 2008 Jun;86(8):1836-45.
  13. Huang CY et al. Biomedicine (Taipei). 2017 Dec;7(4):23.
  14. Zhang MJ et al. Biomed Pharmacother. 2017 Nov 9;97:1131-1137.
  15. Maggioni D et al. Nutr Cancer. 2014;66(7):1257-67.
  16. Yang C et al. Cancer Lett. 2017 Jul 28;399:10-19.
  17. Jo S et al. Anticancer Res. 2017 Apr;37(4):1705-1710.
  18. Li HG et al. J BUON. 2016 Jan-Feb;21(1):182-90.
  19. Xu Y et al. Mol Med Rep. 2016 Mar;13(3):2094-100.
  20. Zang W et al. Tumour Biol. 2014 Dec;35(12):12583-92.
  21. Kim ME et al. Anticancer Res. 2014 Feb;34(2):701-6.
  22. Xu R et al. Food Chem. 2013 May 1;138(1):48-53.
  23. Sun F et al. Nutr Cancer. 2012;64(4):599-606.
  24. Phillips PA et al. Cancer Lett. 2011 Sep 28;308(2):181-8.
  25. Zhang X et al. Zhongguo Zhong Yao Za Zhi. 2010 Apr;35(8):1046-50.
  26. Feng J et al. Mol Cell Biochem. 2015 Oct;408(1-2):163-70.
  27. Lindqvist C et al. Anticancer Res. 2014 Aug;34(8):3975-9.
  28. Devi KP et al. Life Sci. 2015 Dec 1;142:19-25.
  29. Büchter C et al. Int J Mol Sci. 2013 Jun 4;14(6):11895-914.
  30. Drummond NJ et al. Sci Rep. 2017 Sep 19;7(1):11857.
  31. Kreshin S. Life Extension. 2017 Apr.

0 comments :

Post a Comment

All Contents Copyright © 1995-2016 Life Extension® All rights reserved.
Privacy Policy | Terms of Use
*These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease.
The information provided on this site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional or any information contained on or in any product label or packaging. You should not use the information on this site for diagnosis or treatment of any health problem or for prescription of any medication or other treatment. You should consult with a healthcare professional before starting any diet, exercise or supplementation program, before taking any medication, or if you have or suspect you might have a health problem. You should not stop taking any medication without first consulting your physician.