Protective effects of Aster yomena (Kitam.) Honda from cognitive dysfunction induced by high-fat diet

Abstract

In our study, we investigated whether Aster yomena (Kitam.) Honda (AY) improved cognitive impairment which results from consumption of high-fat diet (HFD). When ethyl acetate fraction from AY (EFAY) was administered to C57BL/6J mice fed with 60% HFD, EFAY significantly enhanced cognitive ability that was impaired by HFD in T-maze test and novel object recognition test. Furthermore, EFAY increased memory and learning functions that were proven during Morris water maze test. We further elucidated protective mechanisms of EFAY against cognitive decline that resulted from obesity by western blotting. In the brain, HFD increased neuronal inflammation and disturbed insulin receptor substrate-1 (IRS-1)/Akt pathway. However, EFAY significantly downregulated inflammation-related protein expressions such as nuclear factor-kappa B interleukin-1 beta, inducible nitric oxide synthase and cyclooxygenase-2, compared with the HFD-fed control group. Furthermore, the IRS-1/Akt pathway was regulated by EFAY, indicating that EFAY ameliorated insulin resistance in the brain. Practical applications Obesity and its complications increase the risk for developing cognitive dysfunction such as dementia. Administration of ethyl acetate fraction from AY (EFAY)-attenuated cognitive and memory impairment by inhibitions of neuronal oxidative stress and low-grade chronic inflammation in high-fat diet (HFD)-induced cognitive impairment mouse model. In addition, EFAY-administered mice disturbed cerebral insulin receptor substrate-1 (IRS-1)/Akt pathway. These data suggest that EFAY-improved cognitive impairment induced by HFD through modulation of insulin resistance and inflammation. Therefore, we proposed that AY could be a potential agent to prevent cognitive dysfunction induced by obesity and insulin resistance.