• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

烟酰胺对衰老细胞具有抗氧化作用。

Nicotinamide exerts antioxidative effects on senescent cells.

作者信息

Kwak Ju Yeon, Ham Hyun Joo, Kim Cheol Min, Hwang Eun Seong

机构信息

Department of Life Science, University of Seoul, Seoul 130-743, Korea.

Biochemistry, Pusan National University Medical College, Busan 602-739, Korea.

出版信息

Mol Cells. 2015 Mar;38(3):229-35. doi: 10.14348/molcells.2015.2253. Epub 2015 Jan 19.

DOI:10.14348/molcells.2015.2253
PMID:25600149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4363722/
Abstract

Nicotinamide (NAM) has been shown to suppress reactive oxygen species (ROS) production in primary human fibroblasts, thereby extending their replicative lifespan when added to the medium during long-term cultivation. Based on this finding, NAM is hypothesized to affect cellular senescence progression by keeping ROS accumulation low. In the current study, we asked whether NAM is indeed able to reduce ROS levels and senescence phenotypes in cells undergoing senescence progression and those already in senescence. We employed two different cellular models: MCF-7 cells undergoing senescence progression and human fibroblasts in a state of replicative senescence. In both models, NAM treatment substantially decreased ROS levels. In addition, NAM attenuated the expression of the assessed senescence phenotypes, excluding irreversible growth arrest. N-acetyl cysteine, a potent ROS scavenger, did not have comparable effects in the tested cell types. These data show that NAM has potent antioxidative as well as anti-senescent effects. Moreover, these findings suggest that NAM can reduce cellular deterioration caused by oxidative damage in postmitotic cells in vivo.

摘要

烟酰胺(NAM)已被证明可抑制原代人成纤维细胞中活性氧(ROS)的产生,因此在长期培养过程中添加到培养基中时可延长其复制寿命。基于这一发现,推测NAM通过保持低水平的ROS积累来影响细胞衰老进程。在本研究中,我们探究了NAM是否真的能够降低正在经历衰老进程的细胞以及已经处于衰老状态的细胞中的ROS水平和衰老表型。我们采用了两种不同的细胞模型:正在经历衰老进程的MCF-7细胞和处于复制性衰老状态的人成纤维细胞。在这两种模型中,NAM处理均显著降低了ROS水平。此外,NAM减弱了所评估的衰老表型的表达,但不包括不可逆的生长停滞。N-乙酰半胱氨酸,一种有效的ROS清除剂,在测试的细胞类型中没有类似的作用。这些数据表明NAM具有强大的抗氧化和抗衰老作用。此外,这些发现表明NAM可以减少体内有丝分裂后细胞中由氧化损伤引起的细胞退化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/752eee4afb16/molcell-38-3-229f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/0a09ac6f2a8b/molcell-38-3-229f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/9662b788277f/molcell-38-3-229f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/5a0376b6ca9c/molcell-38-3-229f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/8cf163f0230c/molcell-38-3-229f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/1ee6440ec957/molcell-38-3-229f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/752eee4afb16/molcell-38-3-229f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/0a09ac6f2a8b/molcell-38-3-229f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/9662b788277f/molcell-38-3-229f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/5a0376b6ca9c/molcell-38-3-229f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/8cf163f0230c/molcell-38-3-229f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/1ee6440ec957/molcell-38-3-229f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f98b/4363722/752eee4afb16/molcell-38-3-229f6.jpg

相似文献

1
Nicotinamide exerts antioxidative effects on senescent cells.烟酰胺对衰老细胞具有抗氧化作用。
Mol Cells. 2015 Mar;38(3):229-35. doi: 10.14348/molcells.2015.2253. Epub 2015 Jan 19.
2
Rapamycin Protects Skin Fibroblasts from Ultraviolet B-Induced Photoaging by Suppressing the Production of Reactive Oxygen Species.雷帕霉素通过抑制活性氧的产生保护皮肤成纤维细胞免受紫外线B诱导的光老化。
Cell Physiol Biochem. 2018;46(5):1849-1860. doi: 10.1159/000489369. Epub 2018 Apr 25.
3
Effect of nicotinamide supplementation in in vitro fertilization medium on bovine embryo development.烟酰胺补充剂对体外受精培养液中牛胚胎发育的影响。
Mol Reprod Dev. 2020 Oct;87(10):1070-1081. doi: 10.1002/mrd.23417. Epub 2020 Sep 4.
4
Effect of Antioxidants on the Fibroblast Replicative Lifespan .抗氧化剂对成纤维细胞复制寿命的影响。
Oxid Med Cell Longev. 2020 Sep 23;2020:6423783. doi: 10.1155/2020/6423783. eCollection 2020.
5
AICAR and nicotinamide treatment synergistically augment the proliferation and attenuate senescence-associated changes in mesenchymal stromal cells.AICAR 和烟酰胺联合处理协同增强间充质基质细胞的增殖并减弱与衰老相关的变化。
Stem Cell Res Ther. 2020 Feb 3;11(1):45. doi: 10.1186/s13287-020-1565-6.
6
Creatine and Nicotinamide Prevent Oxidant-Induced Senescence in Human Fibroblasts.肌酸和烟酰胺可预防人成纤维细胞氧化诱导的衰老。
Nutrients. 2021 Nov 16;13(11):4102. doi: 10.3390/nu13114102.
7
A drug-induced accelerated senescence (DIAS) is a possibility to study aging in time lapse.药物诱导的加速衰老(DIAS)是一种在时间推移中研究衰老的可能性。
Age (Dordr). 2014 Jun;36(3):9658. doi: 10.1007/s11357-014-9658-8. Epub 2014 May 16.
8
Metformin lowers the threshold for stress-induced senescence: a role for the microRNA-200 family and miR-205.二甲双胍降低应激诱导衰老的阈值:微小 RNA-200 家族和 miR-205 的作用。
Cell Cycle. 2012 Mar 15;11(6):1235-46. doi: 10.4161/cc.11.6.19665.
9
Progression of genotype-specific oral cancer leads to senescence of cancer-associated fibroblasts and is mediated by oxidative stress and TGF-β.基因型特异性口腔癌的进展导致癌相关成纤维细胞衰老,这是由氧化应激和 TGF-β介导的。
Carcinogenesis. 2013 Jun;34(6):1286-95. doi: 10.1093/carcin/bgt035. Epub 2013 Jan 27.
10
1,8-Cineole promotes G0/G1 cell cycle arrest and oxidative stress-induced senescence in HepG2 cells and sensitizes cells to anti-senescence drugs.1,8-桉叶素促进 HepG2 细胞 G0/G1 期细胞周期阻滞和氧化应激诱导的衰老,并增强细胞对抗衰老药物的敏感性。
Life Sci. 2020 Feb 15;243:117271. doi: 10.1016/j.lfs.2020.117271. Epub 2020 Jan 8.

引用本文的文献

1
Cellular senescence in Alzheimer's disease: from physiology to pathology.阿尔茨海默病中的细胞衰老:从生理学到病理学。
Transl Neurodegener. 2024 Nov 20;13(1):55. doi: 10.1186/s40035-024-00447-4.
2
ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice.ASK-1 激活通过增加肾小球通透性加剧肾功能障碍,并加速糖尿病肾病模型小鼠的细胞衰老。
Sci Rep. 2024 Nov 2;14(1):26438. doi: 10.1038/s41598-024-77577-2.
3
Effect of Selected Antioxidants on the In Vitro Aging of Human Fibroblasts.

本文引用的文献

1
Mitochondrial oxidative stress in aging and healthspan.衰老与健康寿命中的线粒体氧化应激
Longev Healthspan. 2014 May 1;3:6. doi: 10.1186/2046-2395-3-6. eCollection 2014.
2
The interaction between oxidative stress and mast cell activation plays a role in acute lung injuries induced by intestinal ischemia-reperfusion.氧化应激与肥大细胞激活之间的相互作用在肠缺血再灌注引起的急性肺损伤中起作用。
J Surg Res. 2014 Apr;187(2):542-52. doi: 10.1016/j.jss.2013.10.033. Epub 2013 Oct 21.
3
Nicotinamide-induced mitophagy: event mediated by high NAD+/NADH ratio and SIRT1 protein activation.
抗氧化剂对体外培养的人成纤维细胞衰老的影响。
Int J Mol Sci. 2024 Jan 26;25(3):1529. doi: 10.3390/ijms25031529.
4
The Role of Nicotinamide as Chemo-Preventive Agent in NMSCs: A Systematic Review and Meta-Analysis.烟酰胺作为 NMSCs 化学预防剂的作用:系统评价和荟萃分析。
Nutrients. 2023 Dec 27;16(1):100. doi: 10.3390/nu16010100.
5
Integrated Analysis of Transcriptome and Metabolome Profiles in the Longissimus Dorsi Muscle of Buffalo and Cattle.水牛和黄牛背最长肌转录组与代谢组图谱的综合分析
Curr Issues Mol Biol. 2023 Dec 4;45(12):9723-9736. doi: 10.3390/cimb45120607.
6
Impaired Autophagic Flux in Glucose-Deprived Cells: An Outcome of Lysosomal Acidification Failure Exacerbated by Mitophagy Dysfunction.葡萄糖剥夺细胞中的自噬通量受损:溶酶体酸化失败导致的结果,加剧了自噬功能障碍。
Mol Cells. 2023 Nov 30;46(11):655-663. doi: 10.14348/molcells.2023.0121. Epub 2023 Oct 23.
7
Lipofuscin Granule Accumulation Requires Autophagy Activation.脂褐素颗粒积累需要自噬激活。
Mol Cells. 2023 Aug 31;46(8):486-495. doi: 10.14348/molcells.2023.0019. Epub 2023 Jul 13.
8
Effects of nicotinamide on follicular development and the quality of oocytes.烟酰胺对卵泡发育和卵母细胞质量的影响。
Reprod Biol Endocrinol. 2022 Apr 21;20(1):70. doi: 10.1186/s12958-022-00938-x.
9
Creatine and Nicotinamide Prevent Oxidant-Induced Senescence in Human Fibroblasts.肌酸和烟酰胺可预防人成纤维细胞氧化诱导的衰老。
Nutrients. 2021 Nov 16;13(11):4102. doi: 10.3390/nu13114102.
10
Effect of Dry-Aging on Quality and Palatability Attributes and Flavor-Related Metabolites of Pork Loins.干腌熟成对猪里脊肉品质、适口性特征及风味相关代谢物的影响
Foods. 2021 Oct 19;10(10):2503. doi: 10.3390/foods10102503.
烟酰胺诱导的线粒体自噬:由高 NAD+/NADH 比例和 SIRT1 蛋白激活介导的事件。
J Biol Chem. 2012 Jun 1;287(23):19304-14. doi: 10.1074/jbc.M112.363747. Epub 2012 Apr 9.
4
Kinetics of the cell biological changes occurring in the progression of DNA damage-induced senescence.DNA 损伤诱导衰老过程中细胞生物学变化的动力学。
Mol Cells. 2011 Jun;31(6):539-46. doi: 10.1007/s10059-011-1032-4. Epub 2011 Apr 21.
5
A comparative analysis of the cell biology of senescence and aging.衰老与老化细胞生物学的比较分析。
Cell Mol Life Sci. 2009 Aug;66(15):2503-24. doi: 10.1007/s00018-009-0034-2. Epub 2009 May 7.
6
p53-, SIRT1-, and PARP-1-independent downregulation of p21WAF1 expression in nicotinamide-treated cells.烟酰胺处理的细胞中p21WAF1表达的p53、SIRT1和PARP-1非依赖性下调。
Biochem Biophys Res Commun. 2008 Apr 4;368(2):298-304. doi: 10.1016/j.bbrc.2008.01.082. Epub 2008 Jan 28.
7
DNA damage in telomeres and mitochondria during cellular senescence: is there a connection?细胞衰老过程中端粒和线粒体中的DNA损伤:它们有关联吗?
Nucleic Acids Res. 2007;35(22):7505-13. doi: 10.1093/nar/gkm893. Epub 2007 Nov 5.
8
Nicotinamide extends replicative lifespan of human cells.烟酰胺可延长人类细胞的复制寿命。
Aging Cell. 2006 Oct;5(5):423-36. doi: 10.1111/j.1474-9726.2006.00234.x. Epub 2006 Aug 25.
9
Senescence-associated beta-galactosidase is lysosomal beta-galactosidase.衰老相关β-半乳糖苷酶是溶酶体β-半乳糖苷酶。
Aging Cell. 2006 Apr;5(2):187-95. doi: 10.1111/j.1474-9726.2006.00199.x.
10
Effect of N-acetyl-L-cysteine on ROS production and cell death caused by HEMA in human primary gingival fibroblasts.N-乙酰-L-半胱氨酸对人原代牙龈成纤维细胞中HEMA诱导的活性氧生成及细胞死亡的影响。
Biomaterials. 2006 Mar;27(9):1803-9. doi: 10.1016/j.biomaterials.2005.10.022. Epub 2005 Nov 14.