Raisins are an important source of polyphenolic compounds in plant foods, and polyphenols are associated with antioxidant and anti-aging activity. In this work, 628 polyphenols in raisin extracts were characterized using UPLC-MS/MS, mainly including tricetin 3′-glucuronide, diisobutyl phthalate, butyl isobutyl phthalate, isoquercitrin and 6-hydroxykaempferol-7-O-glucoside. The oxidative stress in H₂O₂-induced HepG2 cells and D-gal-induced aging mice was alleviated by raisin polyphenols (RPs) via increases in the cellular levels of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH), along with decreases in malonaldehyde (MDA), reactive oxygen species (ROS) and advanced glycosylation end-products (AGEs) levels. In addition, it was observed that RPs enhanced Sirt1 and Sirt3 expression, initiating the Keap1-Nrf2 signaling pathway, by upregulating the levels of nuclear Nrf2, facilitating the expressions of the antioxidant proteins NQO1 and HO-1, and downregulating Keap1 and cytoplasmic Nrf2 protein levels in H₂O₂-induced HepG2 cells and D-gal-induced aging mice. In summary, RP exerted antioxidant and anti-aging effects via regulating the Sirt1–Nrf2 signaling pathway in vitro and in vivo.

Dried apricots are rich in a variety of polyphenols, which have anti-cancer activity. In this study, 949 phenolic substances were found by means of UPLC-MS/MS, mainly including 2′,7-dihydroxy-3′,4′-dimethoxyisoflavan, scopoletin, rutin, quercetin-3-O-robinobioside, and elaidolinolenic acid. The results indicated that dried apricot polyphenols (DAPs) could cause cell cycle arrest in the G0/G1 and G2/M phases by decreasing the cyclin D1, CDK4, cyclin B1, CDK1, and CDK6 levels in A549 human lung adenocarcinoma cells. Moreover, the ROS and Bax levels were increased, and the Bcl-2 and mitochondrial membrane potential were decreased in A549 cells treated with DAP, increasing caspase-9, caspase-3, and cleaved-PARP1 activities and leading to apoptosis of the A549 cells. Meanwhile, tumor growth was also inhibited by DAPs in an A549 tumor-bearing mouse model, Bax and caspase-3 were upregulated, and Bcl-2 was downregulated, inducing apoptosis of lung cancer cells. In conclusion, DAPs could inhibit lung cancer cell growth by inducing apoptosis due to cell cycle arrest and mitochondria-dependent pathways.