From the Department of Clinical Pharmacology (Magadmi, Nassibi, Kamel, Bakhshwin, Jamal, Alsieni, Burzangi), Department of Physiology (Zaher, Bendary), Faculty of Medicine, from the Department of Medical Laboratory Technology (Al-Rafiah), Faculty of Applied Medical Sciences, King Abdulaziz University, and from the Department of Pharmacy (Nassibi), East Jeddah Hospital, Ministry of Health, Jeddah, Kingdom of Saudi Arabia.
Neurosciences (Riyadh). 2024 May;29(2):103-112. doi: 10.17712/nsj.2024.2.20230060.
To investigate the fundamental mechanisms of the neuroprotective impact of Astaxanthin (AST) in a mouse model of Alzheimer's disease (AD) induced by scopolamine.
This research constituted an in vivo animal study encompassing 36 adult male mice, divided into 6 groups: Control, 100 mg/kg AST, 2 mg/kg scopolamine (AD group), 100 mg/kg AST+2 mg/kg scopolamine, 3 mg/kg galantamine+2 mg/kg scopolamine, and 100 mg/kg AST+3 mg/kg galantamine+2 mg/kg scopolamine. After 14 days, the mice's short-term memory, hippocampus tissue, oxidative and inflammatory markers were evaluated.
The AST demonstrated a beneficial influence on short-term memory and a reduction in acetylcholinesterase activity in the brain. It exhibited neuroprotective and anti-amyloidogenic properties, significantly decreased pro-inflammatory markers and oxidative stress, and reversed the decline of the Akt-1 and phosphorylated Akt pathway, a crucial regulator of abnormal tau. Furthermore, AST enhanced the effect of galantamine in reducing inflammation and oxidative stress.
The findings indicate that AST may offer therapeutic benefits against cognitive dysfunction in AD. This is attributed to its ability to reduce oxidative stress, control neuroinflammation, and enhance Akt-1 and pAkt levels, thereby underscoring its potential in AD treatment strategies.
研究虾青素（AST）在东莨菪碱诱导的阿尔茨海默病（AD）小鼠模型中神经保护作用的基本机制。
这是一项包含 36 只成年雄性小鼠的体内动物研究，分为 6 组：对照组、100mg/kg AST 组、2mg/kg 东莨菪碱（AD 组）、100mg/kg AST+2mg/kg 东莨菪碱组、3mg/kg 加兰他敏+2mg/kg 东莨菪碱组和 100mg/kg AST+3mg/kg 加兰他敏+2mg/kg 东莨菪碱组。14 天后，评估小鼠的短期记忆、海马组织、氧化和炎症标志物。
AST 对短期记忆有有益的影响，并降低了大脑中的乙酰胆碱酯酶活性。它具有神经保护和抗淀粉样变性特性，显著降低了促炎标志物和氧化应激，并逆转了 Akt-1 和磷酸化 Akt 途径的下降，Akt-1 和磷酸化 Akt 途径是异常 tau 的关键调节剂。此外，AST 增强了加兰他敏降低炎症和氧化应激的作用。
研究结果表明，AST 可能对 AD 的认知功能障碍提供治疗益处。这归因于其降低氧化应激、控制神经炎症以及增加 Akt-1 和 pAkt 水平的能力，从而突出了其在 AD 治疗策略中的潜力。
