Beneficial effect of black rice (<em>Oryza</em>&nbsp;<em>sativa</em>&nbsp;<em>L</em>. var.&nbsp;<em>japonica</em>) extract on amyloid &beta;‑induced cognitive dysfunction in a mouse model
Ah Young Lee, Ji Myung Choi, Young‐A Lee, Seon Hwa Shin, Eun Ju Cho
Abstract
Alzheimer's disease (AD) is an age‑dependent progressive neurodegenerative disease, resulting in memory loss and cognitive dysfunction. The accumulation of amyloid β (Aβ) has been identified as the most important risk factor for AD. Black rice (BR; <em>Oryza</em> <em>sativa</em> <em>L</em>. var. <em>japonica</em>), which is widely consumed in Asia, is a good source of bioactive compounds including anthocyanins. Therefore, the aim of the present study was to evaluate the protective effect of BR extracts against Aβ<sub>25‑35</sub>‑induced memory impairment in an <em>in vivo</em> AD mouse model. After intracerebroventricular injection of Aβ<sub>25‑35</sub>, mice were treated with BR extract supplementation for 14 days. Memory and cognition function were evaluated over this period in both treated and untreated animals using T‑maze, novel object recognition and Morris water maze tests. After behavioral tests, malondialdehyde (MDA) and nitric oxide (NO) concentrations in brain, liver and kidney tissues were analyzed. Mice treated with Aβ<sub>25‑35</sub> had impaired memory and cognitive function; however, mice administered BR extract (100 mg/kg/day) demonstrated an improvement in cognition and memory function compared with the Aβ<sub>25‑35</sub>‑injected control group. Furthermore, injection of Aβ<sub>25‑35</sub> significantly increased MDA and NO generation in the brain, liver and kidney of mice. However, the group administered with BR extract had significantly inhibited lipid peroxidation and NO generation in the brain, liver and kidney. In addition, the protective effect of BR on lipid peroxidation and NO production by Aβ<sub>25‑35</sub> was stronger in the brain compared with other tissues. Collectively, these findings suggested that BR supplementation may prevent memory and cognition deficits caused by Aβ<sub>25‑35</sub>‑induced oxidative stress.