衰老
氧化应激
超氧化物歧化酶
体内
生物
丙二醛
KEAP1型
谷胱甘肽过氧化物酶
烟酰胺单核苷酸
生物化学
体外
细胞生物学
烟酰胺腺嘌呤二核苷酸
NAD+激酶
转录因子
酶
生物技术
基因
作者
Xuxin Liu,Tursunay Dilxat,Qiang Shi,Taoyu Qiu,Junping Lin
出处
期刊:Gene
[Elsevier]
日期:2022-05-01
卷期号:822: 146348-146348
被引量:26
标识
DOI:10.1016/j.gene.2022.146348
摘要
Aging is referred to progressive dysfunction of body organs, including the brain. This study aims to explore the anti-aging effect of combing nicotinamide mononucleotide (NMN) and lycopene (Lyco) (NMN + Lyco) on aging rats and senescent PC12 cells. Both in vivo and in vitro aging models were established using D-galactose (D-gal). The combination showed a trend to superiority over monotherapy in preventing aging in vivo and in vitro. Morris water maze test showed that NMN + Lyco effectively improved the ability of spatial location learning and memory of aging model rats. NMN + Lyco mitigated the oxidative stress of rat brains, livers, and PC12 cells by elevating the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), GSH, as well as total antioxidant capacity (T-AOC), and reducing malondialdehyde (MDA) content. CCK-8 assay, senescence-associated β-galactosidase staining, and flow cytometer confirmed the cellular senescence of PC12 cells after exposing D-gal, and indicated the anti-senescence effect of NMN + Lyco in vitro. Moreover, NMN + Lyco effectively down-regulated the expressions of p53, p21, and p16 (senescence-related genes), and activated Keap1-Nrf2 signaling in both in vivo and in vitro aging models. In total, NMN + Lyco protected rats and PC12 cells from cognitive impairment and cellular senescence induced by D-gal, of which effects might be linked to the reduction of oxidative stress and the activation of Keap1-Nrf2 signaling.
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