Aging is typically accompanied by biological and physiological changes that alter cellular functions. Two of the most predominant phenomena in aging include chronic low-grade inflammation (inflammaging) and changes in the gut microbiota composition (dysbiosis). Although a direct causal relationship has not been established, many studies have reported significant reductions in inflammation during aging through well-maintained gut health and microbial balance. Prebiotics and probiotics are known to support gut health and can be easily incorporated into the daily diet. Unfortunately, few studies specifically focus on their significance in reducing inflammation during aging. Therefore, this review summarizes the scientific evidence of the potential roles of probiotics and two types of prebiotics, resistant starch and resistant proteins, in later age. Studies have demonstrated that the oral consumption of bacteria that may contribute to anti-inflammatory response, such as Bifidobacterium spp., Akkermansia munichipilla, and Faecalis praunitzii, contributes significantly to the suppression of pro-inflammatory markers in elderly humans and aged animals. Colonic fermentation of resistant starch and proteins also demonstrates anti-inflammatory activity owing to the production of butyrate and an improvement in the gut microbiota composition. Collectively, probiotics, resistant starch, and resistant proteins have the potential to promote healthy aging.
Chronological aging is commonly accompanied by chronic low-grade inflammation (or “inflammaging”), a contributor to the development of age-related chronic diseases. Aging increases oxidative stress that accelerates telomere shortening, leading to cell senescence and the generation of senescence-associated secretory phenotype (SASP) that exacerbates inflammation. Dietary antioxidants may help protect telomeres and attenuate inflammation. Thyme essential oil (TEO), reported for its potency against neuroinflammation, was fed to chronologically aged C57BL/6J mice for 24 weeks. The TEO diet showed notable impacts on the hippocampus, indicated by lower expression of the aging-related gene p16INK4A (p = 0.0783) and significantly lower expression of cyclin D kinase Cdk4 and Cdk6 (p < 0.05) compared to the age-matched control mice. The TEO group also showed significantly lower gene expression of the pro-inflammatory cytokine Il6 (p < 0.05) in the hippocampus and lower Il1b expression in the liver and cerebellum (p < 0.05). In vitro experiments conducted on NIH-3T3 cells expressing SASP revealed the dose-dependent anti-inflammatory activity of TEO. Remarkably, TEO diet-fed mice showed higher survival rates and significantly longer blood telomere lengths than the control mice. Monoterpene antioxidants in TEO, particularly thymol and p-cymene, may primarily contribute to the anti-inflammatory and telomere-protecting activities of TEO.
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