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首页> 外文期刊>Marine Drugs >Protective Effects of Fucoidan on Aβ25–35 and d -Gal-Induced Neurotoxicity in PC12 Cells and d -Gal-Induced Cognitive Dysfunction in Mice
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Protective Effects of Fucoidan on Aβ25–35 and d -Gal-Induced Neurotoxicity in PC12 Cells and d -Gal-Induced Cognitive Dysfunction in Mice

机译：岩藻聚糖对PC12细胞Aβ25-35和d-Gal诱导的神经毒性的保护作用以及d-Gal诱导的小鼠的认知功能障碍

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease which contributes to memory loss and cognitive decline in the elderly. Fucoidan, extracted from brown algae, is a complex sulfated polysaccharide and potential bioactive compound. In this study, we investigated whether fucoidan protects PC12 cells from apoptosis induced by a combination of beta-amyloid 25–35 (Aβ25–35) and d -galactose ( d -Gal), and improves learning and memory impairment in AD model mice. The results indicated that fucoidan could inhibit the release of cytochrome c from the mitochondria to cytosol and activation of caspases, and increase the expression of apoptosis inhibitor proteins (IAPs), including livin and X-linked IAP (XIAP) in PC12 cells damaged by Aβ25–35 and d -Gal-induction. Fucoidan reversed the decreased activity of acetylcholine (ACh) and choline acetyl transferase (ChAT), as well as the increased activity of acetylcholine esterase (AChE), in AD model mice induced by infusion of d -Gal. Furthermore, fucoidan improved antioxidant activity in vitro and in vivo by activation of superoxide dismutase (SOD) and glutathione (GSH). These results suggested that fucoidan could protect PC12 cells from apoptosis and ameliorate the learning and memory impairment in AD model mice, which appeared to be due to regulating the cholinergic system, reducing oxidative stress, and inhibiting the caspase-dependent apoptosis pathway.
机译：阿尔茨海默氏病（AD）是一种慢性神经退行性疾病，可导致老年人记忆力减退和认知能力下降。从褐藻中提取的岩藻依聚糖是一种复杂的硫酸化多糖，具有潜在的生物活性。在这项研究中，我们研究了岩藻依聚糖是否能保护PC12细胞免受β-淀粉样蛋白25-35（Aβ25-35）和d-半乳糖（d-Gal）的组合诱导的凋亡，并改善AD模型小鼠的学习和记忆障碍。结果表明，岩藻依聚糖可以抑制线粒体细胞色素c向细胞质的释放和胱天蛋白酶的活化，并增加Aβ25损伤的PC12细胞中livin和X连锁IAP（XIAP）等凋亡抑制蛋白（IAP）的表达。 –35和d -Gal归纳法。在输注d-Gal引起的AD模型小鼠中，岩藻糖苷逆转了乙酰胆碱（ACh）和胆碱乙酰基转移酶（ChAT）的活性降低，以及乙酰胆碱酯酶（AChE）的活性增加。此外，岩藻依聚糖通过激活超氧化物歧化酶（SOD）和谷胱甘肽（GSH）改善了体内和体外的抗氧化活性。这些结果表明岩藻依聚糖可以保护PC12细胞免于凋亡并改善AD模型小鼠的学习和记忆障碍，这似乎是由于调节胆碱能系统，降低氧化应激和抑制caspase依赖性凋亡途径所致。

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