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引用本文:江 敏, 徐晓峰, 吴城荔, 于 兰, 罗汉将, 陈 敏.罗汉果苷Ⅴ在帕金森病模型中的神经保护机制研究[J].广西植物,2026,46(3):381-392.[点击复制]
JIANG Min, XU Xiaofeng, WU Chengli, YU Lan, LUO Hanjiang, CHEN Min.Neuroprotective mechanism study of Mogroside V in Parkinson's disease models[J].Guihaia,2026,46(3):381-392.[点击复制]
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罗汉果苷Ⅴ在帕金森病模型中的神经保护机制研究
江 敏, 徐晓峰, 吴城荔, 于 兰, 罗汉将, 陈 敏*   
桂林医科大学第一附属医院神经科学实验室, 广西神经系统疾病临床医学研究中心, 广西数字医学临床转化工程研究中心, 广西 桂林 541001
摘要:
广西特色植物罗汉果是“药食两用”名贵中药材,罗汉果苷V(Mogroside V,MV)是罗汉果中的重要活性成分,具有潜在的神经保护作用,但具体机制尚不清楚。该研究利用α-突触核蛋白(α-synuclein,α-Syn)预成型纤维(preformed fibrils,PFF)处理C57BL/6J胎鼠大脑皮层原代神经元成功建立帕金森病(Parkinson's disease,PD)模型。以MV干预PD原代神经元模型,通过蛋白质免疫印记及细胞免疫荧光方法评估MV对PD关键蛋白α-Syn、多巴胺受体D1(DRD1)及N-甲基-D-天冬氨酸受体NR1亚基(NMDAR1)的作用。此外,结合NMDAR1质粒过表达技术,检测α-Syn、DRD1及NMDAR1的相互关系。结果表明:(1)10 μg·mL-1 α-Syn PFF显著降低原代神经元中DRD1与NMDAR1的表达水平(P<0.05)。(2)100 μmol·L-1 MV处理显著抑制α-Syn PFF导致的原代神经元中DRD1和NMDAR1表达下降(P<0.05)。(3)α-Syn PFF可显著下调DRD1和NMDAR1的表达,而过表达NMDAR1可逆转α-Syn PFF诱导的DRD1表达下调。综上认为,MV通过上调NMDAR1表达,缓解α-Syn导致的DRD1表达下降。该研究结果为阐明MV具有PD神经保护作用提供了新的实验基础,为开发罗汉果及其活性成分MV作为神经保护药物提供了理论依据,为广西特色植物的深度开发和价值提升提供了新的科学路径。
关键词:  罗汉果苷Ⅴ, α-突触核蛋白, 多巴胺受体D1, N-甲基-D-天冬氨酸受体NR1亚基, 帕金森病
DOI:10.11931/guihaia.gxzw202511004
分类号:Q946
文章编号:1000-3142(2026)03-0381-12
基金项目:中央引导地方科技发展资金(桂科ZY23055035); 广西自然科学基金(2025GXNSFAA069132); 国家自然科学基金(82360241, 82304876); 广西研究生教育创新计划项目(YCSW2025473,YCSW2024455)。
Neuroprotective mechanism study of Mogroside V in Parkinson's disease models
JIANG Min, XU Xiaofeng, WU Chengli, YU Lan, LUO Hanjiang, CHEN Min*   
Neuroscience Laboratory, Guangxi Clinical Research Center for Neurological Diseases, Guangxi Engineering Research Center of Digital Medicine and Clinical Translation, The First Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi, China
Abstract:
Siraitia grosvenorii, a characteristic plant of Guangxi, is a precious Chinese medicinal material that can be used both as medicine and food. Mogroside V(MV)is a principal bioactive constituent of S. grosvenorii, possesses potential neuroprotective effects whose mechanisms are not fully understood. In this study, to establish the Parkinson's disease(PD)primary neurons model, primary cortical neurons were isolated from C57BL/6J fetal mice for 7 days' culture, α-synuclein(α-Syn)preformed fibrils(PFF)were added to the cellular cultural medium. Then, 100 μmol·L-1 MV was used to intervene in the PD primary neurons model. After 48 hours' co-treatment, Western blot and cellular immunofluorescence analysis were applied to clarify the effects of MV on the expression of key proteins in PD, such as α-Syn, dopamine receptor D1(DRD1)and N-methyl-D-aspartate receptor NR1 subunit(NMDAR1)in PD primary cortical neurons. Furthermore, to clarify the specific mechanism by which MV affects the expression of DRD1, this study established a PD cell model by adding 10 μg·mL-1 α-Syn PFF to the PC12 cell line. In addition, plasmid transfection technology was utilized to overexpress the NMDAR1 level in PC12 cell line. Western blot and cellular immunofluorescence analysis were also used to evaluate the interrelationship among α-Syn, DRD1 and NMDAR1 in PC12 cells. The results were as follows:(1)10 μg·mL-1 α-Syn PFF significantly decreased the expression levels of DRD1 and NMDAR1 in primary neurons(P<0.05).(2)100 μmol·L-1 MV treatment significantly inhibited the down-regulation of DRD1 and NMDAR1 expression induced by α-Syn PFF in primary neurons(P<0.05).(3)The expression of DRD1 and NMDAR1 were both decreased by α-Syn PFF, while overexpression of NMDAR1 reversed the down-regulation of DRD1 level induced by α-Syn PFF. In conclusion, MV alleviates α-Syn PFF-induced down-regulation of DRD1 level by up-regulating NMDAR1 expression. This study provides a new experimental basis for elucidating the neuroprotective effect of MV on PD, provides a theoretical foundation for the development of S. grosvenorii and its active component MV as neuroprotective drugs, and provides a new scientific path for the in-depth development and value enhancement of Guangxi characteristic plants.
Key words:  Mogroside V, α-synuclein, dopamine receptor D1, N-methyl-D-aspartic acid receptor subunit NR1, Parkinson's disease
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