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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

咖啡因通过调节阿尔茨海默氏症大鼠模型中的神经祖细胞存活和减少氧化应激来改善记忆力和认知

卷 20, 期 3, 2023

发表于: 06 July, 2023

页: [175 - 189] 页: 15

弟呕挨: 10.2174/1567205020666230605113856

价格: $65

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摘要

目的：咖啡因具有有效的抗氧化、抗炎和抗凋亡活性，可对抗多种神经退行性疾病，包括阿尔茨海默病 (AD) 和帕金森病 (PD)。本研究的目的是探讨咖啡因等精神活性物质对链脲佐菌素 (STZ) 诱导的大鼠神经变性的海马神经发生和记忆功能的保护作用。 背景：咖啡因是一种天然的中枢神经系统兴奋剂，属于甲基黄嘌呤类，是一种广泛食用的精神活性物质。据报道，它可以降低与心血管系统（CVS）相关、癌症相关或由于代谢失调引起的各种异常的风险。短期咖啡因暴露已被广泛评估，但其长期暴露却很少被探索和追求。多项研究表明咖啡因在神经退行性疾病中具有毁灭性的作用。然而，咖啡因对神经退行性变的保护作用仍不清楚。 目的：在这里，我们研究了长期服用咖啡因对侧脑室注射 STZ 引起的记忆功能障碍的海马神经发生的影响。通过标记新生细胞的胸苷类似物 BrdU、标记新生细胞的 DCX（未成熟神经元的标记）和标记成熟神经元的 NeuN 共同标记神经元，评估咖啡因对海马神经元增殖和神经元命运决定的长期影响。 方法：第 1 天将 STZ（1 mg/kg，2 μl）立体定向注射到侧脑室（侧脑室内注射）一次，然后用咖啡因（10 mg/kg，腹腔注射）和多奈哌齐（5 mg/kg， i.p.）。评估咖啡因对认知障碍和成人海马神经发生的保护作用。 结果：我们的研究结果表明，STZ 损伤的 SD 大鼠服用咖啡因后，氧化应激负担和淀粉样蛋白负担减少。此外，溴脱氧尿苷/双皮质素 (BrdU /DCX ) 和溴脱氧尿苷 / 神经元核 (BrdU /NeuN ) 的双重免疫标记表明，咖啡因改善了 STZ 损伤大鼠的神经元干细胞增殖和长期存活。 结论：我们的研究结果支持咖啡因在 STZ 诱导的神经变性中具有神经源性潜力。

关键词: 阿尔茨海默氏症，咖啡因，神经发生，海马体，前额叶皮层，莫里斯水迷宫。

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