COP-22 alleviates D-galactose-induced brain aging by attenuating oxidative stress, inflammation and apoptosis in mice

Abstract

Abstract Aging is a natural and inevitable process of organisms. With the intensification of population aging, research on aging has become a hot topic of global attention. The most obvious manifestation of human aging is the aging of brain function, which has been linked to the development of neurodegenerative diseases. In this study, COP-22, a mono-carbonyl curcumin derivative, was evaluated for its anti-aging ability, especially its ability to resist brain aging in mice induced by D-galactose (D-gal). For brain protection, COP-22 could resist D-gal-induced oxidative stress by increasing the activity of anti-oxidative defense enzymes and enhancing antioxidant capacity in the brain tissue; COP-22 could improve the dysfunction of the cholinergic system through decreasing the increased activity of acetylcholinesterase and increasing the reduced content of acetylcholine induced by D-gal; and COP-22 could protect nerve cells of the brain. Further, the western bolt was used to determine related protein of the brain. We found that COP-22 could effectively protect against brain injury (SIRT1, p53, p21 and p16) by inhibiting oxidative stress (Nrf2 and HO-1), inflammation (IL-6 and TNF-α) and apoptosis (Bax and Caspase-3) in D-gal-induced aging mice. Additionally, COP-22 demonstrated the ability to reduce oxidative stress in serum and liver caused by D-gal, as well as relieve the damages of liver and kidney induced by D-gal. These results indicated that COP-22 had potential anti-aging activity, and could be used in the therapy of aging and aging-associated diseases like Alzheimer disease.