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-κB interleukin-1β,
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.