Abstract：
OBJECTIVE: To evaluate whether the glycosylation of chrysin (CHR) enhances its protective effects against aluminum-induced neurotoxicity.
METHODS: To compare the antioxidant, anticholinesterase, and behavioral effects of CHR with its glycosylated form (CHR bonded to β-d-glucose tetraacetate, denoted as LQFM280), we employed an integrated approach using both in vitro (SH-SY5Y cells) and in vivo (aluminum-induced neurotoxicity in Swiss mice) models.
RESULTS: LQFM280 demonstrated higher antioxidant activity than CHR in both models. Specifically, LQFM280 exhibited the ability to exert antioxidant effects in the cytoplasm of SH-SY5Y cells, indicating its competence in traversing neuronal membranes. Remarkably, LQFM280 proved more effective than CHR in recovering memory loss and counteracting neuronal death in the aluminum chloride mice model, suggesting its increased bioavailability at the brain level.
CONCLUSIONS: The glycosylation of CHR with β-d-glucose tetraacetate amplifies its neuroprotective effects, positioning LQFM280 as a promising lead compound for safeguarding against neurodegenerative processes involving oxidative stress.
METHODS: To compare the antioxidant, anticholinesterase, and behavioral effects of CHR with its glycosylated form (CHR bonded to β-d-glucose tetraacetate, denoted as LQFM280), we employed an integrated approach using both in vitro (SH-SY5Y cells) and in vivo (aluminum-induced neurotoxicity in Swiss mice) models.
RESULTS: LQFM280 demonstrated higher antioxidant activity than CHR in both models. Specifically, LQFM280 exhibited the ability to exert antioxidant effects in the cytoplasm of SH-SY5Y cells, indicating its competence in traversing neuronal membranes. Remarkably, LQFM280 proved more effective than CHR in recovering memory loss and counteracting neuronal death in the aluminum chloride mice model, suggesting its increased bioavailability at the brain level.
CONCLUSIONS: The glycosylation of CHR with β-d-glucose tetraacetate amplifies its neuroprotective effects, positioning LQFM280 as a promising lead compound for safeguarding against neurodegenerative processes involving oxidative stress.
摘要：
目的：评估白菊素（CHR）的糖基化是否增强了其对铝诱导的神经毒性的保护作用。
方法：为了比较抗氧化剂，抗胆碱酯酶，和具有糖基化形式的CHR的行为效应（CHR与β-d-葡萄糖四乙酸酯键合，表示为LQFM280)，我们采用了体外(SH-SY5Y细胞)和体内(瑞士小鼠中铝诱导的神经毒性)模型的综合方法.
结果：LQFM280在两种模型中均显示出比CHR更高的抗氧化活性。具体来说,LQFM280显示出在SH-SY5Y细胞的细胞质中发挥抗氧化作用的能力，表明了它穿越神经元膜的能力。值得注意的是,在氯化铝小鼠模型中，LQFM280在恢复记忆丧失和抵消神经元死亡方面比CHR更有效，表明其在大脑水平上的生物利用度增加。
结论：CHR与β-d-葡萄糖四乙酸酯的糖基化增强了其神经保护作用，将LQFM280定位为一种有前途的先导化合物，用于预防涉及氧化应激的神经退行性过程。
方法：为了比较抗氧化剂，抗胆碱酯酶，和具有糖基化形式的CHR的行为效应（CHR与β-d-葡萄糖四乙酸酯键合，表示为LQFM280)，我们采用了体外(SH-SY5Y细胞)和体内(瑞士小鼠中铝诱导的神经毒性)模型的综合方法.
结果：LQFM280在两种模型中均显示出比CHR更高的抗氧化活性。具体来说,LQFM280显示出在SH-SY5Y细胞的细胞质中发挥抗氧化作用的能力，表明了它穿越神经元膜的能力。值得注意的是,在氯化铝小鼠模型中，LQFM280在恢复记忆丧失和抵消神经元死亡方面比CHR更有效，表明其在大脑水平上的生物利用度增加。
结论：CHR与β-d-葡萄糖四乙酸酯的糖基化增强了其神经保护作用，将LQFM280定位为一种有前途的先导化合物，用于预防涉及氧化应激的神经退行性过程。
