An antioxidant suppressed lung cellular senescence and enhanced pulmonary function in aged mice

被引:4
作者
Kawaguchi, Koichiro [1 ]
Hashimoto, Michihiro [1 ,2 ]
Sugimoto, Masataka [1 ,3 ]
机构
[1] Natl Ctr Geriatr & Gerontol, Res Inst, Obu, Aichi 4748511, Japan
[2] Asahikawa Med Univ, Dept Pathol, Div Tumor Pathol, Asahikawa, Hokkaido 0788510, Japan
[3] Grad Sch Med, Dept Mol Aging Res, Nagoya, Aichi 4668560, Japan
关键词
Senescence; NAC; Arf; Aging; Lung;
D O I
10.1016/j.bbrc.2020.12.112
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress is one of the major causes of cellular senescence in mammalian cells. The excess amount of reactive oxygen species generated by oxygen metabolism is pathogenic and facilitates tissue aging. Lung tissue is more susceptible to oxidative stress than other organs because it is directly exposed to environmental stresses. The aging of lung tissues increases the risk of chronic diseases. Senescent cells accumulate in tissues during aging and contribute to aging-associated morbidity; however, the roles of cellular senescence in lung aging and diseases have not yet been elucidated in detail. To clarify the physiological role of oxidative stress-induced cellular senescence in aging-associated declines in pulmonary function, we herein investigated the effects of the antioxidant N-acetyl-Lcysteine (NAC) on lung cellular senescence and aging in mice. The administration of NAC to 1-year-old mice reduced the expression of senescence-associated genes in lung tissue. Pulmonary function and lung morphology were partly restored in mice administered NAC. Collectively, these results suggest that oxidative stress is a major inducer of cellular senescence in vivo and that the control of oxidative stress may prevent lung aging and diseases. (C) 2021 Elsevier Inc. All rights reserved.
引用
收藏
页码:43 / 49
页数:7
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