Opportunities and challenges of foodborne polyphenols applied to anti-aging health foods

Abstract

Abstract: With the increasing proportion of the global aging population, aging mechanisms and anti-aging strategies become hot topics. Nonetheless, the safety of non-natural anti-aging active molecule and the changes in physiological function that occur during aging have not been clarified. There is therefore a need to develop safer pharmaceutical interventions for anti-aging. Numerous types of research have shown that food-derived biomolecules are of great interest due to their unique contribution to anti-aging safety issues and the prevention of degenerative diseases. Among these, polyphenolic organic compounds are widely used in anti-aging research for their ability to mitigate the physiological functional changes that occur during aging. The mechanisms include the free radical theory, immune aging theory, cellular autophagy theory, epigenetic modification theory, gut microbial effects on aging theory, telomere shortening theory, etc. This review elucidates the mechanisms underlying the anti-aging effects of polyphenols found in food-derived bioactive molecules, while also addressing the challenges associated with anti-aging pharmaceuticals. The review concludes by offering insights into the current landscape of anti-aging active molecule research, aiming to serve as a valuable resource for further scholarly inquiry.

Keywords: Anti-aging; Food-derived bioactive molecules; Polyphenols.

Fig. 1

The factors of aging (A). Schematic diagram of antioxidant mechanisms (B). After the addition of polyphenols, the superoxide anion radical (O₂⁻) produced by oxidative stress decreased, and superoxide dismutase (SOD) increased, and the peroxide was converted into H₂O by antioxidant enzymes (NF-κB and Nrf2), glutathione peroxidase (GSH-Px) and catalase (CAT)

Fig. 2

Cell inflammatory signaling pathway transduction mechanisms. During the aging process of young cells, thymus degeneration leads to a decline in immune cell function, decreased T cell proliferation, reduced activity of helper T cells, increased secretion of senescence-associated secretory phenotype (SASP) factors, and enhanced damage-associated molecular patterns (DAMPs) activity. This cascade of events ultimately results in cellular senescence and subsequent bodily senescence

Fig. 3

Mechanisms of the cellular autophagy pathway. The process of autophagy includes initiation, nucleation, elongation, fusion, and degradation. The ULK1-FIP200-ATG13 complex is involved in regulating the induction and initiation of autophagy, and the nucleation of autophagosomes is mainly regulated by Class III PI3K complex composed of Vps34, Atg14L, Beclin-1 and Vps15. The elongation of autophagosomes requires the involvement of ubiquitin-like protein systems, Atg3 and Atg7/LC3. Finally, under the action of lysosomal hydrolase, the bound cargos are degraded, such as invading bacteria, aggregated proteins and damaged organelles

Fig. 4

Intestinal microbial conduction mechanism. Following the consumption of foodborne polyphenols, there is an observed elevation in the abundance of Gram-negative bacteria in the gastrointestinal tract, as well as an increase in the production of lipopolysaccharides (LPS). This results in the translocation of these molecules across the intestinal barrier and into the systemic circulation, facilitating the activation of chronic inflammatory cytokines