乌尔瓦多糖通过调节炎症,氧化损伤和肠道微生物群来缓解帕金森病
Wenqian Wang1, Qingfu Zhang1, Tong Zhang1
1Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin, 300457, PR China; Tianjin Key Laboratory of Industrial Microbiology, Tianjin, 300457, PR China; College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, PR China.
International journal of biological macromolecules
|December 30, 2025
概括
乌尔瓦乳糖多糖 (UPE) 通过减少炎症和氧化应激,显示出对帕金森病 (PD) 的保护作用. 这种天然化合物也积极调节肠道微生物群,为神经退行性疾病提供新的治疗途径.
科学领域:
- 药理学 药理学是指药理学的学科.
- 神经科学是一个神经科学.
- 海洋生物技术 海洋生物技术
背景情况:
- 帕金森病 (PD) 治疗效果有限,副作用严重.
- 肠-大脑轴,炎症和氧化应激是新型PD治疗的关键目标.
- 肠道微生物群失生症在PD病变发生过程中越来越被认可.
研究的目的:
- 在帕金森病模型中研究Ulva lactuca多糖 (UPE) 的神经保护作用.
- 阐明UPE治疗潜力的基础机制,包括其对氧化应激,炎症和肠道微生物群的影响.
主要方法:
- 在体外测试中评估了UPE对1-甲基-4-烯 (MPP+) 诱导毒性的细胞保护作用.
- 在体内研究中使用MPTP诱导的帕金森病小鼠模型.
- 分析包括运动功能测试,多巴胺基神经元评估,氧化应激和炎症标志物量化,肠道微生物群概况 (16SrRNA测序) 和信号通路分析 (Nrf2/HO-1,TLR4/NF-κB).
主要成果:
- 在实验室中,UPE证明了细胞保护作用,减少了细胞亡和氧化应激.
- 在体内,口服UPE给药改善了MPTP治疗小鼠的运动缺陷和多巴胺基神经元损失.
- UPE抑制了全身炎症,质细胞激活和氧化应激标志物.
- UPE调节了肠道微生物群组成,增加了有益的细菌,减少了有害的细菌.
- UPE的机制涉及Nrf2/HO-1和TLR4/NF-κB信号通路的调节.
结论:
- 乌尔瓦乳糖多糖 (UPE) 对帕金森病具有显著的神经保护性.
- 通过减轻氧化应激,减少炎症和积极改变肠道微生物群组成来发挥其作用.
- 这些发现凸显了UPE等天然多糖的治疗潜力,用于治疗神经退行性疾病.
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