엉겅퀴의 스코폴라민 유도 인지능 손상에 대한 개선 효과 및 보호 기전 탐색

초록

Scopolamine induces cholinergic dysfunction and oxidative stress, which leads to cognitive impairment. In the present study, we investigated the mechanisms by which Cirsium japonicum var. maackii (CJM) improved cognitive impairment in scopolamine-injected mice. Mice were administered an ethyl acetate fraction of CJM (EACJM, 50 and 100 mg/kg) for 14 days, and were injected intraperitoneally with scopolamine (1.5 mg/kg) for 8 days. To determine the protective effect of EACJM against memory loss in mice, T-maze, novel object recognition (NOR), and Morris water maze (MWM) tests were conducted using a scopolamine-treated mouse model. The protective mechanisms of EACJM in the brain were studied using western blotting. Scopolamine-induced memory dysfunction in mice was confirmed using behavioral tests, including T-maze, NOR, and MWM. However, results showed that EACJM effectively alleviated memory impairment in scopolamine-treated mice. Brain weight of EACJM-treated mice increased compared to that of scopolamine-injected mice. EACJM also downregulated acetylcholinesterase and upregulated brain-derived neurotrophic factor and phosphorylated cAMP response element-binding protein, indicating that EACJM ameliorated scopolamine-induced cognitive impairment. In addition, EACJM downregulated the B-cell lymphoma-2-associated X protein/ B-cell lymphoma-2 ratio, indicating that EACJM blocked the apoptosis of neuronal cells. These results indicated that EACJM may be a useful therapeutic agent for preventing cognitive impairment in neurodegenerative diseases.

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