Melatonin decreases the expression of inflammation and apoptosis markers in the lung of a senescence-accelerated mice model

被引:29
作者
Puig, Angela [1 ]
Rancan, Lisa [1 ]
Paredes, Sergio D. [2 ]
Carrasco, Adrian [1 ]
Escames, Germaine [3 ]
Vara, Elena [1 ]
Tresguerres, Jesus A. F. [2 ]
机构
[1] Univ Complutense Madrid, Sch Med, Dept Biochem & Mol Biol 3, Avda Complutense S-N, E-28040 Madrid, Spain
[2] Univ Complutense Madrid, Sch Med, Dept Physiol, Avda Complutense S-N, E-28040 Madrid, Spain
[3] Univ Granada, Inst Biotechnol, Ctr Biomed Invest, Edificio Fray Luis de Granada C Ramon & Cajal 4, Granada 18003, Spain
关键词
Aging; Lung; Melatonin; Inflammation; Oxidative stress; Apoptosis; OVARIECTOMIZED FEMALE RATS; VASCULAR ENDOTHELIAL-CELLS; OXIDATIVE STRESS; HEME OXYGENASE-1; AIRWAY INFLAMMATION; LIPID-PEROXIDATION; GENE-EXPRESSION; MURINE MODEL; TNF-ALPHA; MOUSE SAM;
D O I
10.1016/j.exger.2015.11.021
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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-alpha, IL-1 beta, NF kappa B2, HO-1) and apoptosis parameters (BAD, BAX, AIF) in the lung tissue of male senescence-accelerated prone mice (SAMP8). In addition, RNAoxidative damage, as the formation of 8-hydroxyguanosine (8-OHG), was also evaluated. Young andoldanimals, aged 2 and 10 months respectively, were divided into 4 groups: untreated young, untreated old, old mice treated with 1 mg/kg/day melatonin, and old animals treated with 10 mg/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-alpha, IL-1 beta, NF kappa B2, 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 b 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. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:1 / 7
页数:7
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