红柳苷衍生物SHPL-49的神经保护机制包括改善脑脂质代谢紊乱以减轻pMCAO大鼠模型中的铁下垂

Q3 Pharmacology, Toxicology and Pharmaceutics

Phytomedicine Plus Pub Date : 2025-08-14 DOI:10.1016/j.phyplu.2025.100871

Ruyi Wang, Yue Shen, Dong Xie, Zhirui Zheng, Yuying Zhu, Pei Zhang, Jiange Zhang

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引用次数: 0

摘要

缺血性脑卒中发病率高、死亡率高，严重危害人类健康。本研究探讨了红景天苷衍生物SHPL-49 （NB-SHPL-49-A-3，补充材料1）的神经保护作用。永久性大脑中动脉闭塞（pMCAO）的雄性Sprague-Dawley大鼠分别以60 mg/kg和90 mg/kg剂量口服SHPL-49，连续14天，丁苯酞（NBP）为阳性对照。在体内，评估神经功能、梗死面积、认知能力和握力，并分析脂质代谢和与铁中毒相关的ACSL4-GPX4通路。体外建立PC12细胞氧糖剥夺（OGD）模型。结果显示，90mg /kg SHPL-49可通过ACSL4-GPX4途径改善大鼠神经功能和认知功能，减少梗死面积，调节脂质代谢，抑制铁下垂。结论：90 mg/kg口服SHPL-49对缺血性脑卒中大鼠神经退行性变和脂质代谢紊乱具有保护作用。

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Neuroprotective mechanism of salidroside derivative SHPL-49 involves amelioration of brain lipid metabolism disorder to mitigate ferroptosis in a rat model of pMCAO

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Neuroprotective mechanism of salidroside derivative SHPL-49 involves amelioration of brain lipid metabolism disorder to mitigate ferroptosis in a rat model of pMCAO

Ischemic stroke, characterized by high incidence and mortality, severely endangers human health. This study investigated the neuroprotective potential of salidroside derivative SHPL-49 (NB-SHPL-49-A-3, Supplementary Material 1). Male Sprague-Dawley rats with permanent middle cerebral artery occlusion (pMCAO) received oral SHPL-49 at 60 mg/kg and 90 mg/kg for 14 days, with Butylphthalide (NBP) as a positive control. In vivo, neurological function, infarct volume, cognitive ability, and grip strength were evaluated, and lipid metabolism and the ferroptosis-related ACSL4-GPX4 pathway were analyzed. In vitro PC12 cell oxygen-glucose deprivation (OGD) models were established. Results showed that 90 mg/kg SHPL-49 significantly improved neurological and cognitive functions, reduced infarct volume, regulated lipid metabolism, and inhibited ferroptosis via the ACSL4-GPX4 pathway. In conclusion, 90 mg/kg oral SHPL-49 protected against neurodegeneration and reversed lipid metabolism disorder in ischemic stroke rats.

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