Al-Amin Md Mamun, Reza Hasan Mahmud, Saadi Hasan Mahmud, Mahmud Waich, Ibrahim Abdirahman Adam, Alam Musrura Mefta, Kabir Nadia, Saifullah A R M, Tropa Sarjana Tarannum, Quddus A H M Ruhul
Department of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, Bangladesh.
Department of Pharmaceutical Sciences, North South University, Bashundhara, Dhaka, Bangladesh.
Eur J Pharmacol. 2016 Apr 15;777:60-9. doi: 10.1016/j.ejphar.2016.02.062. Epub 2016 Feb 27.
Aluminum chloride induces neurodegenerative disease in animal model. Evidence suggests that aluminum intake results in the activation of glial cells and generation of reactive oxygen species. By contrast, astaxanthin is an antioxidant having potential neuroprotective activity. In this study, we investigate the effect of astaxanthin on aluminum chloride-exposed behavioral brain function and neuronal oxidative stress (OS). Male Swiss albino mice (4 months old) were divided into 4 groups: (i) control (distilled water), (ii) aluminum chloride, (iii) astaxanthin+aluminum chloride, and (iv) astaxanthin. Two behavioral tests; radial arm maze and open field test were conducted, and OS markers were assayed from the brain and liver tissues following 42 days of treatment. Aluminum exposed group showed a significant reduction in spatial memory performance and anxiety-like behavior. Moreover, aluminum group exhibited a marked deterioration of oxidative markers; lipid peroxidation (MDA), nitric oxide (NO), glutathione (GSH) and advanced oxidation of protein products (AOPP) in the brain. To the contrary, co-administration of astaxanthin and aluminum has shown improved spatial memory, locomotor activity, and OS. These results indicate that astaxanthin improves aluminum-induced impaired memory performances presumably by the reduction of OS in the distinct brain regions. We suggest a future study to determine the underlying mechanism of astaxanthin in improving aluminum-exposed behavioral deficits.
氯化铝在动物模型中诱发神经退行性疾病。有证据表明，摄入铝会导致神经胶质细胞激活并产生活性氧。相比之下，虾青素是一种具有潜在神经保护活性的抗氧化剂。在本研究中，我们调查了虾青素对暴露于氯化铝的行为脑功能和神经元氧化应激（OS）的影响。将雄性瑞士白化小鼠（4月龄）分为4组：（i）对照组（蒸馏水），（ii）氯化铝组，（iii）虾青素+氯化铝组，以及（iv）虾青素组。进行了两项行为测试；放射状臂迷宫测试和旷场试验，并在治疗42天后从脑和肝组织中检测OS标志物。暴露于铝的组在空间记忆表现和焦虑样行为方面显著降低。此外，铝组在脑中的氧化标志物；脂质过氧化（MDA）、一氧化氮（NO）、谷胱甘肽（GSH）和蛋白质氧化产物高级氧化（AOPP）显著恶化。相反，虾青素与铝联合给药显示出空间记忆、运动活性和OS得到改善。这些结果表明，虾青素可能通过降低不同脑区的OS来改善铝诱导的记忆障碍。我们建议未来开展一项研究以确定虾青素改善铝暴露行为缺陷的潜在机制。
