Review Volume 15, Issue 23 pp 14473—14505

Traditional herbs: mechanisms to combat cellular senescence

Lei Wang1,2, *, , Jiahui Wang2, *, , Zhihui Yang2, , Yue Wang2, , Tiejian Zhao3, , Weisheng Luo4, , Tianjian Liang2, , Zheng Yang2, ,

  • 1 Graduate School, Guangxi University of Chinese Medicine, Nanning, Guangxi 530222, China
  • 2 Department of Medicine, Faculty of Chinese Medicine Science Guangxi University of Chinese Medicine, Nanning, Guangxi 530222, China
  • 3 Department of Physiology, College of Basic Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi 530222, China
  • 4 Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi 530000, China
* Equal contribution

Received: June 30, 2023       Accepted: October 15, 2023       Published: December 5, 2023      

https://doi.org/10.18632/aging.205269
How to Cite

Copyright: © 2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Cellular senescence plays a very important role in the ageing of organisms and age-related diseases that increase with age, a process that involves physiological, structural, biochemical and molecular changes in cells. In recent years, it has been found that the active ingredients of herbs and their natural products can prevent and control cellular senescence by affecting telomerase activity, oxidative stress response, autophagy, mitochondrial disorders, DNA damage, inflammatory response, metabolism, intestinal flora, and other factors. In this paper, we review the research information on the prevention and control of cellular senescence in Chinese herbal medicine through computer searches of PubMed, Web of Science, Science Direct and CNKI databases.

Abbreviations

TERT: telomerase reverse transcriptase; TBA: thiobarbituric acid; DDR: DNA damage response; ROS: reactive oxygen species; HG: high glucose; NPC: nucleus pulposus cells; SOD: superoxide dismutase; MDA: malondialdehyde; 8-OH-dG: 8-hydroxy-2-deoxyguanosine; MMPs: matrix metalloproteinases; MT: mitochondrial; PI3K: phosphatidylinositol 3-kinase; Akt: protein kinase B; mTOR: mammalian target of rapamycin; D-Gal: d-galactose; UVB: ultraviolet radiation B; AhR: aryl hydrocarbon receptor; SIRTs: sirtuins; NF-κB: nuclear factor-κB protein; AMPK: AMP-activated protein kinase; HIF-1α: hypoxia-inducible factor 1α; HUVEC: human umbilical vein endothelial cells; MTORC1: mTOR complex 1; FMN: formononetin; PGC-1α: peroxisome proliFerators-activated receptor γ coactivator lalpha; PINK1: PTEN-induced kinase 1; IL-6: interleukin 6; IL-1β: interleukin 1β; TLRs: toll-like receptors; BLM: bleomycin; PM2. 5: particulate matter2. 5; T2DM: type 2 diabetes mellitus; Mieap: mitochondrial phagocytic protein; CR: calorie restriction; STR: sweet taste receptors; T1R2: taste receptor family 1 member 2; Gα: α-gustadusin; TRPM5: transient receptor potential cation channel subfamily member 5; SCFAs: short-chain fatty acids; NAFLD: non-alcoholic fatty liver disease; IPF: idiopathic pulmonary fibrosis; EPCs: endothelial progenitor cells; AngII: angiotensin II; MAPK: mitogen-activated protein kinase; JNK: c-Jun amino-terminal kinase; ERK5: extracellular signal-regulated kinase 5; PPARγ: peroxisome proliferator-activated receptor γ; GSH: glutathione; NADPH: nicotinamide adenine dinucleotide phosphate; NOX: nicotinamide adenine dinucleotide phosphate oxidase; NRF2: nuclear factor erythroid-derived 2; Notch1: neurogenic locus notch homolog protein 1; PRR: pattern recognition receptor; NLRs: nod-like receptor proteins; HPMC: human peritoneal mesothelial cells; NPC: nucleus pulposus cells; CSE: cigarette smoke extract; NP: nucleus pulposus; STAT: signal transduction and activator of transcription; DSS: dextran sodium sulfate; TNBS: trinitrobenzenesulfonic acid; STAT17: signal transduction and activator of transcription 17; IRAK3: interleukin-1 receptor-associated kinase 3; SREBPs: scholesterol regulatory element binding proteins; PPARα: peroxisome proliferator-activated receptor α; VSMC: vascular smooth muscle cell; TBHP: tert-butyl hydroperoxide; HDF: human dermal fibroblasts; AQP1: aquaporin 1; RhoA: ras homolog family member A; ROCK: rho-related protein kinase; TG: triacylglycerol; TC: serumtotalcholesterol; PGK1: phosphoglycerate kinase 1; TBI: traumatic brain injury; TNF: tumor necrosis factor; HSCs: hepatic stellate cells; APJendogenouslig: apelin; STZ: streptozotocin; EVO: evodiamine; HSC/HPC: hematopoietic stem cell/hematopoietic progenitor cell; TBHP: tert-butyl hydroperoxide; I/R: ischemia/reperfusion; H/R: hypoxia/reoxygenation; GPX4: glutathione peroxidase 4; GAS5: growth arrest specific 5; lncRNAs: long non-coding RNAs.