Melatonin, a well-known antioxidant molecule that supports healthy inflammation, may protect lung health threatened by viral and other pathogens. A recent study produced data showing that melatonin may act to protect lung health, and could benefit COVID-19 patients.
The study authors suggest that excessive inflammation, oxidation, and an exaggerated immune response very likely contribute to COVID-19 pathology, leading to a cytokine storm and subsequent progression to further health complications. Their article summarizes the likely benefits that melatonin may offer.
Melatonin is not directly antagonistic to pathogens, but it has indirect antagonistic actions due to its pro-healthy inflammation, anti-oxidation and immune enhancing features. Melatonin has been linked to protecting the lung when otherwise vulnerable to oxidative injury, pro-inflammatory cytokine release and inflammatory cell recruitment.
Melatonin is known to support healthy inflammation effects through various pathways, as well as showing anti-oxidative actions that up-regulate anti-oxidative enzymes, down-regulate pro-oxidative enzymes, and possibly exert a direct action of scavenging free radicals.
Previous studies have also demonstrated an immunomodulating effect of melatonin, improving proliferation and maturation of natural killer cells, T and B lymphocytes, granulocytes and monocytes. Researchers have also noted that melatonin showed promising results regarding the attenuation of circulating cytokines.
Considering the role of melatonin in these various physiological processes, a patient’s melatonin levels could possibly be linked to a higher vulnerability to health complications due to viruses, as seen in the elderly population with lower melatonin levels due to aging.
The primary study authors suggest that, although the direct evidence of melatonin application in COVID-19 is unclear, both its use in experimental animal models and in studies on humans has documented its efficacy and safety and that its use by COVID-19 patients may be beneficial.
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