Exploring the Prospective Role of Propolis in Modifying Aging Hallmarks

Abstract

Aging populations worldwide are placing age-related diseases at the forefront of the research agenda. The therapeutic potential of natural substances, especially propolis and its components, has led to these products being promising agents for alleviating several cellular and molecular-level changes associated with age-related diseases. With this in mind, scientists have introduced a contextual framework to guide future aging research, called the hallmarks of aging. This framework encompasses various mechanisms including genomic instability, epigenetic changes, mitochondrial dysfunction, inflammation, impaired nutrient sensing, and altered intercellular communication. Propolis, with its rich array of bioactive compounds, functions as a potent functional food, modulating metabolism, gut microbiota, inflammation, and immune response, offering significant health benefits. Studies emphasize propolis' properties, such as antitumor, cardioprotective, and neuroprotective effects, as well as its ability to mitigate inflammation, oxidative stress, DNA damage, and pathogenic gut bacteria growth. This article underscores current scientific evidence supporting propolis' role in controlling molecular and cellular characteristics linked to aging and its hallmarks, hypothesizing its potential in geroscience research. The aim is to discover novel therapeutic strategies to improve health and quality of life in older individuals, addressing existing deficits and perspectives in this research area.

Keywords: age-related diseases; aging; propolis.

Figure 1

Hallmarks of aging and age-related alterations. The hallmarks of aging, including genomic instability, telomere attrition, aberrant autophagy, gut microbiota imbalance, mitochondrial dysfunction, epigenetic modifications, altered nutrient-sensing pathways, impaired protein homeostasis, and disrupted intercellular communication, are deeply interconnected. These same factors seem to be root cause contributors to age-related diseases. The particular factors and sequences that trigger the shift from the normal changes of aging to the onset of age-related diseases remain unknown.

Figure 2

Biological activities of propolis. Abbreviations: ABCA1, ATP-binding cassette subfamily A member 1; ABCG1, ATP-binding cassette (ABC) subfamily G member 1; AGEs, advanced glycation end products; Bax, bcl-2-like protein 4; Bcl-2, B cell lymphoma 2; CAT, catalase; CD, cluster of differentiation; COX; cyclooxygenase; CXCL-2, chemokine (C-X-C motif) ligand 2; ERK, extracellular signal-regulated kinase; FOXP3, forkhead box P3; G6Pase, glucose-6-phosphatase; GPx, glutathione peroxidase; HbA1C, hemoglobin A1C; HDL, high-density lipoprotein; HO-1, heme oxygenase-1; HOMA-IR, homeostasis model assessment-estimated insulin resistance; iNOS, inducible nitrogen oxide synthase; IFN, interferon; IL, interleukin; JAK2/STAT3, Janus kinase 2/signal transducer and activator of transcription 3; JNK, Jun kinase; LDL, low-density lipoprotein; LOX; lipoxygenase; LXRs, liver X receptors; MDA, malondialdehyde; mTOR, mammalian target of rapamycin; MT1-MMP, membrane type 1-matrix metalloproteinase; miR143, microRNA 143; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NK, natural killer cells; Nrf2, nuclear factor erythroid 2-related factor 2; PPARγ, peroxisome proliferator-activated receptor gamma; PARP, poly (ADP-ribose) polymerase; p53, tumor protein p53; PI3K/AKT, phosphatidylinositol 3-kinase/ protein kinase B; PKC, protein kinase C; PON1, paraoxonase-1; RAGE, receptor for AGEs; regulatory T cells (Tregs); ROS, reactive oxygen species; SCFAs, short-chain fatty acids; SOD, superoxide dismutase; TG, triglyceride; VEGF, vascular endothelial growth factor; VLDL-c, very-low-density lipoprotein cholesterol. The up and down arrows indicate an increase or reduction in the mentioned components.