| Summary: | In order to explore the anti-aging effects of two tocopherol ester derivatives, the in vitro antioxidant capacity of D-α-tocopherol acetate and DL-α-tocopherol acetate was determined. A mouse model of D-galactose-induced was created and intervened with each of the tocopherol ester derivatives for 42 days. Changes in aging related indicators were analyzed. The results showed that the hydroxyl radical scavenging capacity, and the 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) cation radical scavenging capacity, Fe2+ chelating capacity, and total reducing power of the two tocopherol ester derivatives were better than those of vitamin C in the concentration range of 0.1 to 0.3 mg/mL. Compared with the aging model group, after intervention with tocopherol ester derivatives, the content of malondialdehyde (MDA) in serum decreased significantly (P < 0.05, P < 0.01, P < 0.001, and P < 0.000 1), and glutathione peroxidase (GSH-Px) activity and total antioxidant capacity (T-AOC) increased significantly (P < 0.05, P < 0.01, P < 0.001, and P < 0.000 1). The serum levels of inflammatory cytokines such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and liver function indexes including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) decreased significantly (P < 0.05, P < 0.01, P < 0.001, and P < 0.001). Moreover, the relative mRNA and protein expression levels of nuclear factor-E2-related factors (Nrf2), quinone oxidoreductase (NQO1) and heme oxygenase 1 (HO-1) in the mouse liver were enhanced. DL-α-tocopherol acetate increased the relative mRNA expression of Nrf2, NQO1 and HO-1 by 514.08%, 461.78% and 515.32%, respectively, and their relative protein expression by 620.00%, 988.89% and 1 200.00%, respectively (P < 0.000 1). To sum up, the two tocopherol ester derivatives have anti-aging effects on D-galactose-induced aging in mice, DL-α-tocopherol acetate being more effective than D-α-tocopherol acetate, and their anti-aging effects may be related to the regulation of the Nrf2 signaling pathway.
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