Neuropharmacology · 2025
Astragaloside Ⅳ improves neuroinflammation in Parkinson's disease by regulating amino acid metabolism and the PI3K-AKT signaling pathway.
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Liu Lianmei, Li Zhixin, Qin Xuemei, Xu Lei, Li Zhenyu, Xiao Shengnan
Аннотация
OBJECTIVE: Elucidation the pharmacological mechanism of AS-Ⅳ, providing a scientific basis for the development of AS-Ⅳ as a therapeutic agent for Parkinson's disease (PD).
METHODS: An acute PD model was established in C57BL/6 mice through intraperitoneal injection of MPTP. A comprehensive multi-omics approach was employed for in-depth data analysis and processing. The effects of AS-Ⅳ on motor dysfunction and neuropathological changes were validated at both protein and mRNA levels using Western blotting and RT-qPCR, revealing its therapeutic potential and mechanisms of action in PD.
RESULTS: AS-Ⅳ significantly improved behavioral parameters in PD mouse models, increased the population of dopaminergic neurons, and attenuated neuroinflammation. Metabolomic analysis revealed that AS-Ⅳ exerts anti-neuroinflammatory effects through modulation of amino acid metabolism. Further investigation demonstrated that AS-Ⅳ downregulates CCN3 gene expression, thereby enhancing PI3K-AKT phosphorylation and suppressing the expression of inflammatory factors.
CONCLUSIONS: In summary, this study elucidates a novel mechanism of AS-Ⅳ in PD treatment, providing a scientific foundation for the development of AS-Ⅳ drugs for PD.
METHODS: An acute PD model was established in C57BL/6 mice through intraperitoneal injection of MPTP. A comprehensive multi-omics approach was employed for in-depth data analysis and processing. The effects of AS-Ⅳ on motor dysfunction and neuropathological changes were validated at both protein and mRNA levels using Western blotting and RT-qPCR, revealing its therapeutic potential and mechanisms of action in PD.
RESULTS: AS-Ⅳ significantly improved behavioral parameters in PD mouse models, increased the population of dopaminergic neurons, and attenuated neuroinflammation. Metabolomic analysis revealed that AS-Ⅳ exerts anti-neuroinflammatory effects through modulation of amino acid metabolism. Further investigation demonstrated that AS-Ⅳ downregulates CCN3 gene expression, thereby enhancing PI3K-AKT phosphorylation and suppressing the expression of inflammatory factors.
CONCLUSIONS: In summary, this study elucidates a novel mechanism of AS-Ⅳ in PD treatment, providing a scientific foundation for the development of AS-Ⅳ drugs for PD.