Accumulating evidence has suggested that oxidative stress and apoptosis are involved in the ageing process. D-galactose (gal) has been reported to cause symptoms of ageing in rats, accompanied by liver and brain injuries. Our study aimed to investigate the potential antioxidative, anti-inflammatory and anti-apoptotic effects of ellagic acid and to explore how these effects act on rats in a D-gal-induced ageing model. Ageing was induced by subcutaneous injection of D-gal (100 mg/kg/d for 8 weeks). Ellagic acid was simultaneously administered to the D-gal-induced ageing rats once daily by intragastric gavage. Finally, the mental condition, body weight, organ index, levels of inflammatory cytokines, antioxidative enzymes, and liver function, as well as the expression of pro- and anti-apoptotic proteins, were monitored. Our results showed that ellagic acid could improve the mental condition, body weight, organ index and significantly decrease the levels of inflammatory cytokines, normalize the activities of antioxidative enzymes, and modulate the expression of apoptotic protein in ageing rats. In conclusion, the results of this study illustrate that ellagic acid was suitable for the treatment of some ageing-associated problems, such as oxidative stress, and had beneficial effects for age-associated diseases.

Despite tremendous advances in modern medicine, effective prevention or therapeutic strategies for age-related neurodegenerative diseases such as Alzheimer's disease (AD) remain limited. Currently, accumulating evidence has demonstrated that microRNAs (miRNAs) are increasingly associated with age-related diseases and are emerging as promising therapeutic targets. Urolithin A, a metabolite compound resulting from the transformation of ellagitannins by gut bacteria, has been reported to have anti-oxidant, anti-inflammatory, and anti-apoptotic properties. The present study primarily focused on the ameliorative effect of urolithin A on aging mice and on the exploration of the potential mechanisms of such an ameliorative effect on cognitive impairment and brain aging. In this study, we first tested the neuroprotective effect of urolithin A using an in vitro H 2 O 2-induced PC12 cell oxidative damage model. The in vivo D-gal-induced brain aging model showed that urolithin A significantly suppressed the upregulation of miR-34a induced by D-gal. Moreover, target genes associated with miR-34a were also examined. Urolithin A supplementation ameliorated apoptosis induced by D-gal and rescued miR-34a overexpression-induced impaired autophagy in brain aging mice after a 2-month administration. Furthermore, urolithin A activated autophagy by upregulating the SIRT1 signaling pathway and downregulating the mTOR signaling pathway. In conclusion, urolithin A may exert neuroprotective effects and may aid in preventing D-gal-induced brain aging through activation of the miR-34a-mediated SIRT1/mTOR signaling pathway.

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