神经保护
疾病
线粒体
医学
变性(医学)
药理学
生物
化学
神经退行性变
神经元
细胞生物学
黄芪
神经元变性
程序性细胞死亡
运动神经元
自噬
发病机制
炎症
细胞凋亡
线粒体DNA
多糖
退行性疾病
氧化应激
作者
Zewei Cong,Chan Li,Mengqin Sun,Yan Yu,Xianmei Zhang
出处
期刊:PubMed
日期:2026-01-15
卷期号:: 25033-25033
摘要
BACKGROUND: possesses antioxidant, anti-inflammatory, and neuroprotective properties. APS was previously revealed to exert neuroprotective effects in experimental PD models. However, the underlying mechanism remains poorly understood. Therefore, our study was designed to reveal the molecular mechanism through which APS exerts neuroprotective effects in PD. METHODS: -knockout (CEND1-KO) mice were used to confirm whether APS exhibits the neuroprotective effects via a CEND1-dependent mechanism. Behavior tests, immunohistochemical staining, and western blotting were performed to examine mouse motor dysfunction, neuronal injury, and mitochondrial dysfunction. RESULTS: . APS administration successfully improved motor deficits, neuronal injury, and mitochondrial impairments in WT (wild-type) mice, but failed to protect against PD in CEND1-KO mice. CONCLUSION: APS exerts its neuroprotective effects in PD by preventing mitochondrial dysfunction through increasing CEND1 expression.
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