Curculigoside, a traditional Chinese medicine monomer, ameliorates oxidative stress in Alzheimer's disease mouse model via suppressing ferroptosis,Phytotherapy Research

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Curculigoside, a traditional Chinese medicine monomer, ameliorates oxidative stress in Alzheimer's disease mouse model via suppressing ferroptosis
Phytotherapy Research ( IF 6.1 ) Pub Date : 2024-03-06 , DOI: 10.1002/ptr.8152
Yuhang Gong ₁ , Yanan Wang ₁ , Yanfeng Li ₁ , Fanglin Weng ₁ , Tong Chen ₁ , Ling He ₁

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Alzheimer's disease (AD) is a neurodegenerative disorder where oxidative stress, induced by ferroptosis, has been linked to neuronal damage and cognitive deficits. The objective of this study is to investigate if the potential therapeutic agent, Curculigoside (CUR), could ameliorate AD by inhibiting ferroptosis. The potential therapeutic targets, such as GPX4 and SLC7A11, were identified using weighted gene co‐expression network analysis (WGCNA). Concurrently, CUR was also screened against these potential targets using various analytical methods. For the in vivo studies, intragastric administration of CUR significantly ameliorated cognitive impairment in AD model mice induced by scopolamine and okadaic acid (OA). In vitro, CUR protected neuronal cells by altering the levels of ferroptosis‐related specific markers in OA and scopolamine‐induced neurotoxicity. The administration of CUR through intragastric route significantly reduced the levels of AD‐promoting factors (such as Aβ1–42, p‐tau) and ferroptosis‐promoting factors in the hippocampus and cortex of AD mice. Furthermore, CUR up‐regulated the expression of GPX4 and decreased the expression of SLC7A11 in the ferroptosis signaling pathway, thereby increasing the ratio of glutathione (GSH)/oxidized glutathione (GSSG) in vivo and vitro. In conclusion, the cumulative results suggest that the natural compound CUR may serve as a promising therapeutic agent to ameliorate AD by inhibiting ferroptosis.

中文翻译：

中药单体仙茅苷通过抑制铁死亡改善阿尔茨海默病小鼠模型的氧化应激

阿尔茨海默病 (AD) 是一种神经退行性疾病，由铁死亡引起的氧化应激与神经元损伤和认知缺陷有关。本研究的目的是调查潜在的治疗剂仙茅苷 (CUR) 是否可以通过抑制铁死亡来改善 AD。使用加权基因共表达网络分析 (WGCNA) 确定了潜在的治疗靶点，例如 GPX4 和 SLC7A11。同时，还使用各种分析方法针对这些潜在目标筛选 CUR。在体内研究中，灌胃 CUR 可显着改善东莨菪碱和冈田酸 (OA) 诱导的 AD 模型小鼠的认知障碍。在体外，CUR 通过改变 OA 中与铁死亡相关的特异性标记物的水平和东莨菪碱诱导的神经毒性来保护神经元细胞。通过灌胃途径给予 CUR 显着降低了 AD 促进因子（如 Aβ 1–42 , p-tau) 和 AD 小鼠海马和皮质中的铁死亡促进因子。此外，CUR在铁死亡信号通路中上调GPX4的表达并降低SLC7A11的表达，从而增加体内和体外谷胱甘肽（GSH）/氧化型谷胱甘肽（GSSG）的比率。总之，累积的结果表明，天然化合物 CUR 可以作为一种有前途的治疗剂，通过抑制铁死亡来改善 AD。

更新日期：2024-03-06

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