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来自Euphorbia pseudomollis的synagrantol A对LPS诱导的神经炎症的保护作用和机制
Qingwen Hu1, Dan Zhang1, Hanxuan Wang1
1School of Pharmacy, Faculty of Medicine, Macau University of Science and Technology, Macau, Macau SAR, 999078, China; Laboratory of Drug Discovery from Natural Resources and Industrialization, Macau University of Science and Technology, Macau, China.
Journal of ethnopharmacology
|December 5, 2025
概括
这项研究表明,来自Euphorbia pseudomollis的A3化合物有效地减少动物模型中的神经炎症和相关行为障碍. A3 抑制微质激活和炎症通路,为神经系统疾病提供潜在的治疗益处.
科学领域:
- 药理学和民族植物学
- 神经科学和炎症研究研究
- 药物发现和天然产品的发现.
背景情况:
- 传统上使用Euphorbia物种的抗炎和止痛特性.
- 神经炎症与各种神经系统疾病有关.
- 来自Euphorbia pseudomollis的3,4,12,13-Tetraacetyl-20-phenylacetylphorbol (A3) 显示出抗炎作用. 这种药物具有抗炎作用.
研究的目的:
- 研究A3在调节脂聚糖 (LPS) 诱导的神经炎症方面的潜力.
- 评估A3对神经炎症标志物和通路的体外和体内影响.
主要方法:
- 使用UPLC,LC-MS,QTOF和NMR进行A3的化学表征.
- 用BV2微质细胞进行体外研究,评估细胞活力,氧化 (NO) 和炎症性细胞因子.
- 在小鼠体内研究涉及LPS给药,A3治疗,行为测试 (OFT) 和组织病理学分析.
主要成果:
- A3被确定为Euphorbia pseudomollis提取物中的关键成分.
- 在体外,A3剂量依赖地降低了BV2细胞中LPS诱导的NO产生和iNOS表达.
- 在体内,A3治疗改善了LPS诱导的身体衰退,焦虑和运动缺陷,减少了神经炎症和器官病理.
结论:
- 通过抑制微质激活和炎症介质,A3表现出显著的抗神经炎症作用.
- A3降低了NF-κB信号通路的基因表达,这在神经炎症中至关重要.
- A3减轻与LPS诱导的神经炎症相关的行为和病理障碍.
关键词:
3,4,12,13-Tetraacetyl-20-phenylacetylphorbol-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-3-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl-phenylacetyl细胞因子 (cytokines) 是一种细胞因子.这种情绪是 euforbia.微细胞激活活动在NF-κB信号传输中.神经炎症是一种神经炎症.
