多组学分析揭示了提取物对小鼠帕金森病的神经保护作用。
Multi-omics analysis reveals the neuroprotective effect of extract against Parkinson's disease in mouse.
机构信息
Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Health Sciences, Gyeongsang National University, Jinju 52727, Republic of Korea.
2 College of Veterinary Medicine and BK21 FOUR Program, Chonnam National University, Gwangju 61186, Republic of Korea.
出版信息
J Tradit Chin Med. 2024 Dec;44(6):1111-1117. doi: 10.19852/j.cnki.jtcm.2024.06.002.
OBJECTIVE
To assess (ARE) neuroprotective function in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice and related genes.
METHODS
Examined mRNA-DNA methylation changes induced by ARE in MPTP-induced Parkinson's disease (PD) model's substantia nigra.
RESULTS
ARE mitigated MPTP-induced motor impairment in rotarod and open field tests and preserved tyrosine hydroxylase-positive neuronal cells in substantia nigra and striatum. Genome RNA-Sequencing and Methyl-Sequencing in substantia nigra of vehicle/ARE-treated MPTP-induced PD mice showed 84 differentially expressed genes (DEGs) and 1804 differentially methylated regions (DMRs). Upregulated genes involved zinc ion homeostasis, cilium protein localization, and transcription; downregulated genes linked to ephrin receptor signaling, somitogenesis, and gene expression regulation. Hyper/hypomethylated DMRs post-ARE treatment associated with Wnt signaling, mitochondrial organization, dopamine biosynthesis, and hindbrain development. No significant correlation between DEGs and methylated genes related to PD pathogenesis.
CONCLUSION
This research has identified the epigenetic targets of ARE's therapeutic action and gives insight on how ARE protects neurons in Parkinson's disease.
目的
评估 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）处理的小鼠中的神经保护功能和相关基因。
方法
检测 ARE 诱导的 mRNA-DNA 甲基化变化在 MPTP 诱导的帕金森病（PD）模型黑质中的作用。
结果
ARE 减轻了 MPTP 诱导的旋转棒和旷场试验中的运动障碍，并且保存了黑质和纹状体中的酪氨酸羟化酶阳性神经元细胞。车辆/ARE 处理的 MPTP 诱导的 PD 小鼠黑质中的全基因组 RNA 测序和甲基化测序显示 84 个差异表达基因（DEGs）和 1804 个差异甲基化区域（DMRs）。上调的基因涉及锌离子稳态、纤毛蛋白定位和转录；下调的基因与 Eph 受体信号、体节形成和基因表达调控有关。ARE 治疗后的高/低甲基化 DMRs 与 Wnt 信号、线粒体组织、多巴胺生物合成和后脑发育有关。DEGs 和与 PD 发病机制相关的甲基化基因之间没有显著相关性。
结论
这项研究确定了 ARE 治疗作用的表观遗传靶点，并深入了解了 ARE 如何保护帕金森病中的神经元。
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