Cited by 37Circadian rhythm and melatoninGenetics, Aging, and Longevity in Model OrganismsAntioxidants, Aging, Portulaca oleracea

Melatonin Decreases the Expression of Inflammation and Apoptosis Markers in the Lung of a Senescence-Accelerated Mice Model

Puig, Ángela, Rancan, Lisa, Paredes, Sergio D., Carrasco, Adrián, Escames, Germaine, Vara, Elena, Tresguerres, Jesús A.F.·2016·Experimental Gerontology

Abstract

Aging is associated with an increase in oxidative stress and inflammation. The aging lung is particularly affected since it is continuously exposed to environmental oxidants while antioxidant machinery weakens with age. Melatonin, a free radical scavenger, counteracts inflammation and apoptosis in healthy cells from several tissues. Its effects on the aging lung are, however, not yet fully understood. This study aimed to investigate the effect of chronic administration of melatonin on the expression of inflammation markers (TNF-α, IL-1β, NFκB2, HO-1) and apoptosis parameters (BAD, BAX, AIF) in the lung tissue of male senescence-accelerated prone mice (SAMP8). In addition, RNA oxidative damage, as the formation of 8-hydroxyguanosine (8-OHG), was also evaluated. Young and old animals, aged 2 and 10 months respectively, were divided into 4 groups: untreated young, untreated old, old mice treated with 1mg/kg/day melatonin, and old animals treated with 10mg/kg/day melatonin. Untreated young and old male senescence accelerated resistant mice (SAMR1) were used as controls. After 30 days of treatment, animals were sacrificed. Lungs were collected and immediately frozen in liquid nitrogen. mRNA and protein expressions were measured by RT-PCR and Western blotting, respectively. Levels of 8-OHG were quantified by ELISA. Mean values were analyzed using ANOVA. Old nontreated SAMP8 animals showed increased (p<0.05) mRNA and protein levels of TNF-α, IL-1β, NFκB2, and HO-1 compared to young mice and SAMR1 mice. Melatonin treatment with either dose reversed the aging-derived inflammation (p<0.05). BAD, BAX and AIF expressions also rose with aging, the effect being counteracted with melatonin (p<0.05). Aging also caused a significant elevation (p<0.05) in SAMP8 8-OHG values. This increase was not observed in animals treated with melatonin (p<0.05). In conclusion, melatonin treatment was able to modulate the inflammatory and apoptosis status of the aging lungs, exerting a protective effect on age-induced damage.

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Crossref · 10.1016/j.exger.2015.11.021

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  • In vivo, melatonin intake diminishes age-derived inflammation and apoptosis, decreases lipid peroxidation, TBARS, and protein carbonyls, counteracting hippocampal senescence and exerting anti-aging and antioxidant effects on mice brains.

    “In vivo, melatonin intake has been reported to diminish age-derived inflammation and apoptosis and to decrease lipid peroxidation, thiobarbituric acid reactive substances and protein carbonyls, thus counteracting hippocampal senescence and exerting an anti-aging and antioxidant effect on mice brains [462,463,464,465].”

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Authors
Puig, Á., Rancan, L., Paredes, S. D., Carrasco, A., Escames, G., Vara, E., & Tresguerres, J. A. F.
Affiliations
  • Universidad Complutense de Madrid (ES)
  • Universidad de Granada (ES)
Corresponding author
Tresguerres, Jesús A.F.
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2016-03
Volume
75
Pages
1-7
ISSN
0531-5565 (ISSN-L)
OpenAlex
W654580105
Cited by
37
References
44
Citations by year
2026: 1 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 3 · 2018: 7 · 2017: 7
FWCI
2.59
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
Keywords
melatonin, lung aging, senescence-accelerated mice, SAMP8 mice, inflammation, apoptosis, oxidative stress, 8-hydroxyguanosine, TNF-α, IL-1β, NF-κB2, heme oxygenase-1, Bad, Bax, AIF, antioxidant defense
MeSH terms
Aging, Animals, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Evaluation, Preclinical, Gene Expression Regulation, Lung, Male, Melatonin, Mice, Mutant Strains, Biomarkers, Apoptosis, Oxidative Stress, Inflammation Mediators, Aging, Premature

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