Nanoliposomal curcumin protects against D-galactose-induced hepatic aging by targeting oxidative stress, mitochondrial dysfunction, and inflammatory signaling.

OBJECTIVES

With advancing age, individuals experience a decline in liver function, an increase in oxidative stress, and diminished mitochondrial efficiency. This research examined the protective effects of curcumin (CUR), in both free and nanoliposomal (CUR-LNP) forms, against D-galactose (D-gal)-induced liver aging in male Wistar rats.

METHODS

Rats were assigned to six groups: control, CUR, CUR-LNPs, D-gal, D-gal+CUR, and D-gal+CUR-LNPs. CUR and CUR-LNPs (40 mg/kg) and D-gal (150 mg/kg) were administered orally for 10 weeks. Liver function, lipid profile, oxidative stress (GSH, CAT, SOD, and NRF2/HO-1), mitochondrial function (ATP and respiratory complexes), inflammation (NF-κB, TNF-α, IL-1β, IL-6, and iNOS), and apoptosis (caspases, Bax/Bcl-2) were assessed. Histological and ultrastructural analyses were also performed.

KEY FINDINGS: D-gal induced hepatic injury, oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis. CUR partially attenuated these alterations, whereas CUR-LNPs produced greater protection by restoring liver enzymes and lipid homeostasis, enhancing antioxidant and mitochondrial functions, suppressing NF-κB signaling and inflammatory mediators, and reducing apoptotic markers. Histological and ultrastructural analyses confirmed preserved hepatocyte and mitochondrial architecture.

CONCLUSION

CUR, especially in its nanoliposomal form, exerts potent hepatoprotective, antioxidant, anti-inflammatory, and anti-apoptotic effects against D-gal-induced liver aging, supporting its potential as a therapeutic strategy for age-related hepatic dysfunction.