Torularhodin from Attenuates d-galactose/AlCl-Induced Cognitive Impairment, Oxidative Stress, and Neuroinflammation via the Nrf2/NF-κB Pathway.

Oxidative stress and neuroinflammation are considered as crucial culprits in Alzheimer's disease (AD). Torularhodin, a carotenoid pigment, possesses powerful antioxidant activity. This study aimed to elucidate the protective effects of torularhodin in the AD-like mouse model and investigated the underlying mechanisms. Behavioral and histopathological results suggested that torularhodin relieved cognitive impairments, attenuated Aβ accumulation, and inhibited glial overactivation in d-gal/AlCl-induced ICR mice. Simultaneously, torularhodin also markedly increased antioxidant enzyme capacities, lowered the contents of RAGE, and reduced levels of inflammatory cytokines. Western blot results showed that torularhodin ameliorated neuronal oxidative damage via activation of Nrf2 translocation, upregulation of HO-1, and inactivation of NF-κB in vivo and in vitro. Thus, torularhodin effectively ameliorated cognitive impairment, oxidative stress, and neuroinflammation, possibly through the Nrf2/NF-κB signaling pathways, suggesting torularhodin might offer a promising prevention strategy for neurodegenerative diseases.