Blackcurrant Attenuates D-Galactose-Induced Oxidative Damage in Mice through Regulating the Keap1-Nrf2/ARE Pathway

To investigate the antioxidant effect of blackcurrant using a D-galactose-induced oxidative injury mouse model and to explore the underlying mechanism.

Sixty healthy C57BL/6J mice were randomly divided into six groups (n = 10 per group): blank control, model control, positive control, and low-, medium-, and high-dose blackcurrant groups. All groups except the blank control group received intraperitoneal injections of D-galactose for 10 weeks to establish the model, followed by the corresponding interventions for 4 weeks. During the experiment, body mass was monitored. At the end of the experiment, oxidative stress-related indicators in serum, liver, and brain tissues were measured. Liver histopathological sections were examined, the mRNA expression levels of P16 and P21 in brain tissues were detected, and the expression of genes related to the Kelch-like ECH-associated protein 1-nuclear factor erythroid-2 related factor 2/antioxidant response element (Keap1-Nrf2/ARE) signaling pathway in the liver was assessed.

Blackcurrant intervention significantly ameliorated oxidative stress, as evidenced by increased activities of superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GSH-Px) in the serum and liver, along with decreased levels of malondialdehyde (MDA) and protein carbonyl (PC). Additionally, blackcurrant effectively alleviated pathological damage in liver tissues, downregulated the mRNA expression of P16 and P21 in brain tissues, and upregulated the expression of Nrf2 pathway-related genes (such as glutathione-S-transferases (GST) and heme oxygenase-1 (HO-1)) in the liver.

Blackcurrant exerts antioxidant effects and alleviates liver and brain injury induced by D-galactose by reducing the level of oxidative stress. The antioxidant effects of blackcurrant may be mediated by regulating the Keap1-Nrf2/ARE signaling pathway.