Department of Food Science and Nutrition, Pusan National University, Busan, Republic of Korea.
Department of Food Science, Gyeongsang National University, Jinju, Republic of Korea.
J Food Biochem. 2022 Jul;46(7):e14138. doi: 10.1111/jfbc.14138. Epub 2022 Mar 23.
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.
在我们的研究中，我们调查了 Aster yomena（Kitam.）Honda（AY）是否改善了高脂肪饮食（HFD）引起的认知障碍。当从 AY（AY 乙酸乙酯馏分，EFAY）给予喂食 60%HFD 的 C57BL/6J 小鼠时，EFAY 显著增强了 T 迷宫测试和新物体识别测试中 HFD 引起的认知能力损伤。此外，EFAY 提高了在 Morris 水迷宫测试中证明的记忆和学习功能。我们通过蛋白质印迹进一步阐明了 EFAY 对肥胖引起的认知下降的保护机制。在大脑中，HFD 增加了神经元炎症并干扰了胰岛素受体底物-1（IRS-1）/Akt 通路。然而，与 HFD 喂养的对照组相比，EFAY 显著下调了炎症相关蛋白的表达，如核因子-κB、白细胞介素-1β、诱导型一氧化氮合酶和环氧化酶-2。此外，IRS-1/Akt 通路受 EFAY 调节，表明 EFAY 改善了大脑中的胰岛素抵抗。实际应用：肥胖及其并发症增加了发展为认知功能障碍（如痴呆）的风险。AY 乙酸乙酯馏分（EFAY）的给药通过抑制高脂肪饮食（HFD）诱导的认知障碍小鼠模型中的神经元氧化应激和低度慢性炎症，减轻了认知和记忆损伤。此外，给予 EFAY 的小鼠干扰了大脑胰岛素受体底物-1（IRS-1）/Akt 通路。这些数据表明，EFAY 通过调节胰岛素抵抗和炎症改善了 HFD 引起的认知障碍。因此，我们提出 AY 可以成为预防肥胖和胰岛素抵抗引起的认知功能障碍的潜在药物。
