在斑马鱼模型中,Karanjin对双A诱导的认知缺陷和氧化损伤的保护作用
B Logeshwari1, Srikanth Jeyabalan2, Gayathri Veeraraghavan3
1Department of Pharmacology, Sri Ramachandra Faculty of Pharmacy, Sri Ramachandra Institute of Higher Education and Research (DU), Porur, Chennai, 600116, Tamil Nadu, India.
Scientific reports
|September 26, 2025
概括
卡兰金是一种天然化合物,有效地逆转了斑马鱼中双A (BPA) 引起的神经毒性. 它表现出显著的神经保护作用,恢复认知功能和减少氧化应激,这表明神经退行性疾病的治疗潜力.
科学领域:
- 神经科学是一个神经科学.
- 环境健康 环境健康
- 药理学 药理学是指药理学的学科.
背景情况:
- 双A (BPA) 是一种内分泌干扰物,与神经毒性,认知衰退和阿尔茨海默氏症等神经退行性疾病有关.
- BPA通过氧化应激,线粒体功能障碍和神经炎症诱导神经毒性.
- 斑马鱼 (Danio rerio) 作为一种有价值的模型生物来研究神经退行性疾病.
研究的目的:
- 为了研究卡兰金对斑马鱼中双A (BPA) 诱导的神经毒性的神经保护潜力.
- 评估卡兰金在逆转BPA诱导的行为和生化缺陷方面的疗效.
- 为了比较Karanjin的神经保护作用与标准的神经保护剂.
主要方法:
- 成年斑马鱼被暴露在BPA (4毫克/升) 中21天.
- 斑马鱼随后接受了不同剂量的卡拉宁 (5 mg/L和10 mg/L) 的治疗.
- 作为比较剂,神经保护剂donepezil和mentat被使用.
- 进行了行为测试 (新型坦克潜水,T迷宫,新型物体识别,Y迷宫),生物化学测试 (AChE,GSH,SOD,LPO) 和组织病理学评估.
主要成果:
- 暴露于BPA显著损害了斑马鱼的探索行为,学习和记忆.
- 高剂量卡拉金治疗逆转了BPA诱导的行为缺陷.
- 暴露于BPA增加了乙胆化酶 (AChE) 活性和脂质过氧化 (LPO),并降低了谷氨酸 (GSH) 和超氧化失调酶 (SOD) 水平.
- 卡兰金治疗显著降低了ACHE活性和LPO,同时恢复了GSH和SOD水平.
- 组织病理学分析证实了Karanjin能够保持神经元完整性的能力.
结论:
- 卡兰金在斑马鱼中表现出显著的神经保护作用,对抗BPA诱导的神经毒性.
- 卡兰金表现出强大的抗氧化和抗炎性质,减轻BPA诱导的神经元损伤.
- 这些发现表明,卡兰金作为神经退行性疾病的治疗药物具有前途,与现有的药物相比.
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