Experimental study demonstrates fucoxanthin mitigates hepatic damage and senescence in aging mice, highlighting its therapeutic potential for age-related liver health.
Key Points
To investigate the protective effects and underlying molecular mechanisms of the marine carotenoid fucoxanthin against liver injury in an accelerated aging mouse model.
Mice were subjected to daily intraperitoneal injections of 400 mg/kg d-galactose for 12 weeks to induce accelerated aging.
Treatment groups received concurrent daily oral gavage of fucoxanthin at doses of 50 mg/kg or 100 mg/kg for 12 weeks.
Fucoxanthin significantly attenuated liver injury by decreasing serum ALT and AST levels, reducing DNA damage, and down-regulating cellular senescence markers including p53, p21, p16, and β-galactosidase.
Fucoxanthin suppressed oxidative stress by lowering reactive oxygen species, malondialdehyde, and protein carbonyls while restoring catalase, superoxide dismutase, and glutathione peroxidase activities.
Treatment inhibited hepatic inflammation via suppression of the NF-κB signaling pathway and blocked intrinsic apoptosis, RIPK1/RIPK3/MLKL-mediated necroptosis, and NLRP3/caspase-1/GSDMD-driven pyroptosis cascades.