Anthocyanins Delay D‐Galactose–Induced Mouse Liver Aging by Regulating the <scp>NF</scp> ‐ <scp>κB</scp> / <scp>IKK</scp> Signaling Pathway

Aging is an intricate pathophysiological phenotype. It is the result of the combined action of various inflammatory factors and cytokines. Aging is closely related to inflammation, apoptosis, tumors, and other diseases. Anthocyanins are a kind of natural flavonoid, mainly contained in plant fruits such as bilberry, grape, purple sweet potato, and so on. These flavonoids have antioxidation, antiaging, and anti-inflammatory properties. It has been found that anthocyanins can effectively delay liver, ovary, and other organ aging. However, the biological mechanism by which anthocyanins alleviate aging phenotypes is still poorly understood. To simulate liver aging in mice, D-galactose was injected daily at 800 mg/kg to accelerate aging, and anthocyanins at 20 or 40 mg/kg were given as intervention treatments. The antiaging effect of anthocyanins was evaluated by body weight, inflammatory markers, and aging markers. Serum ALT and AST levels were measured, and liver histology was assessed using hematoxylin-eosin staining. In addition, we explored the molecular mechanism of anthocyanins delaying liver aging by detecting the expression levels of NF-κB/IKK signaling protein molecules. Our results indicate that anthocyanins can effectively delay mouse liver senescence induced by D-galactose. Analyses by Western blot demonstrated that anthocyanins inhibited the NF-κB/IKK signaling pathway, thereby inhibiting inflammation. In vitro, anthocyanins attenuate the D-galactose (D-gal)-induced aging in AML12 cells, as indicated by reduced aging-associated p21 and p16. Anthocyanins can similarly inhibit the NF-κB/IKK signal pathway in D-gal-induced aging in AML12 cells. Based on these findings, anthocyanins reduce liver aging in mice by regulating the NF-κB/IKK pathway.