Oxidative stress and neuroinflammation are considered as crucial culprits in Alzheimer's diseases (AD). Torularhodin, a carotenoid pigment, possesses powerful antioxidant activity. This study aimed to elucidate the protective effects of… Click to show full abstract
Oxidative stress and neuroinflammation are considered as crucial culprits in Alzheimer's diseases (AD). Torularhodin, a carotenoid pigment, possesses powerful antioxidant activity. This study aimed to elucidate the protective effects of torularhodin in AD-like model and investigated the underlying mechanisms. Behavior tests and histopathological results suggested that torularhodin relieved D-gal/AlCl3-stimulated cognitive impairments, attenuated Aβ accumulation, and glial overactivation in the mice brain. Simultaneously, torularhodin also markedly increased antioxidant enzyme capacities, lower the contents of RAGE, and reduced levels of inflammatory cytokines. Western blots 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 in neurodegenerative diseases.
               
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