Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Xiaoyao San alleviates abnormal α‑syn aggregation and neuronal injury in a Caenorhabditis elegans model of Parkinson disease via the SKN-1 antioxidative pathway].
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Ye Lixuan, Liao Yuxin, Liu Qiong, Zhang Jia, Gao Lei, Dong Zhaoyang
Аннотация
OBJECTIVES: To investigate the neuroprotective effects of XiaoyaoSan (XYS) in a Caenorhabditis elegans (C. elegans) model of Parkinson disease (PD) and explore its molecular mechanism.
METHODS: A PD model was established in C. elegans using 6-hydroxydopamine (6-OHDA) and validated using a transgenic strain overexpressing α‑synuclein (α‑syn) (NL5901). The worms were treated with 25, 50 or 100 μg/mL XYS, and their lifespan was recorded. Their motor function and food-related behaviors were evaluated by counting body bends within 20 s and observing the basal slowing response. Dopaminergic neuron degeneration and α‑syn aggregation were observed in GFP-labeled transgenic worms. Intracellular ROS levels were measured using a DHE fluorescent probe, and the mRNA expressions of dat-1, cat-2, ced-9, gst-4, and sod-3 were analyzed using RT-qPCR. RNA interference (RNAi) was employed to knock down skn-1 expression to determine whether the effects of XYS depend on the SKN-1/Nrf2 signaling pathway.
RESULTS: XYS significantly prolonged the lifespan of PD model worms, increased their body bends within 20 s on day 5 and day 10, and improved the basal slowing response. XYS obviously alleviated 6-OHDA-induced dopaminergic neuronal damage, upregulated the expression of dat-1, cat-2, and ced-9, and reduced α‑syn accumulation. Treatment with XYS decreased reactive oxygen species (ROS) levels and upregulated the antioxidant-related genes including sod-3 and gst-4. Mechanistic studies showed that XYS significantly enhanced skn-1::GFP and sod-3::GFP fluorescence signals. Knocking down skn-1 resulted in decreased lipid content in the worms, and XYS failed to significantly reverse this change; skn-1 knockdown also abolished the restorative effect of XYS on sod-3::GFP fluorescence reduction.
CONCLUSIONS: XYS improves neurological function in Caenorhabditis elegans PD model by alleviating oxidative stress and suppressing abnormal α‑syn aggregation, and its neuroprotective effect is mediated probably by the SKN-1/Nrf2-related antioxidant pathway.
METHODS: A PD model was established in C. elegans using 6-hydroxydopamine (6-OHDA) and validated using a transgenic strain overexpressing α‑synuclein (α‑syn) (NL5901). The worms were treated with 25, 50 or 100 μg/mL XYS, and their lifespan was recorded. Their motor function and food-related behaviors were evaluated by counting body bends within 20 s and observing the basal slowing response. Dopaminergic neuron degeneration and α‑syn aggregation were observed in GFP-labeled transgenic worms. Intracellular ROS levels were measured using a DHE fluorescent probe, and the mRNA expressions of dat-1, cat-2, ced-9, gst-4, and sod-3 were analyzed using RT-qPCR. RNA interference (RNAi) was employed to knock down skn-1 expression to determine whether the effects of XYS depend on the SKN-1/Nrf2 signaling pathway.
RESULTS: XYS significantly prolonged the lifespan of PD model worms, increased their body bends within 20 s on day 5 and day 10, and improved the basal slowing response. XYS obviously alleviated 6-OHDA-induced dopaminergic neuronal damage, upregulated the expression of dat-1, cat-2, and ced-9, and reduced α‑syn accumulation. Treatment with XYS decreased reactive oxygen species (ROS) levels and upregulated the antioxidant-related genes including sod-3 and gst-4. Mechanistic studies showed that XYS significantly enhanced skn-1::GFP and sod-3::GFP fluorescence signals. Knocking down skn-1 resulted in decreased lipid content in the worms, and XYS failed to significantly reverse this change; skn-1 knockdown also abolished the restorative effect of XYS on sod-3::GFP fluorescence reduction.
CONCLUSIONS: XYS improves neurological function in Caenorhabditis elegans PD model by alleviating oxidative stress and suppressing abnormal α‑syn aggregation, and its neuroprotective effect is mediated probably by the SKN-1/Nrf2-related antioxidant pathway.
Предметные рубрики MeSH
AnimalsCaenorhabditis elegansalpha-SynucleinCaenorhabditis elegans ProteinsTranscription FactorsDNA-Binding ProteinsDrugs, Chinese HerbalParkinson DiseaseDisease Models, AnimalReactive Oxygen SpeciesAnimals, Genetically ModifiedSignal TransductionDopaminergic NeuronsNeuroprotective AgentsOxidative StressOxidopamineAntioxidants