首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production
【2h】

Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production

机译:紫锥菊苷可通过减少ROS的产生来保护6-羟基多巴胺诱导的线粒体功能障碍和PC12细胞的炎症反应。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction and inflammatory responses are involved in the mechanism of cell damage in PD. 6-Hydroxydopamine (6-OHDA), a dopamine analog, specifically damages dopaminergic neurons. Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems of Cistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.
机译:帕金森氏病(PD)是一种神经退行性疾病,其特征在于黑质中多巴胺能(DA)神经元的进行性丧失。线粒体功能障碍和炎症反应与PD细胞损伤的机制有关。多巴胺类似物6-羟基多巴胺(6-OHDA)特别会损伤多巴胺能神经元。紫锥菊苷(ECH)是从肉stan蓉肉的茎中分离出来的一种苯乙胺类苷,在以前的研究中显示出多种神经保护作用。本研究旨在研究其对6-OHDA诱导的神经毒性的作用及其在PC12细胞中的可能机制。结果表明,与未处理的PC12细胞相比,6-OHDA降低了细胞活力,降低了氧化还原活性,降低了线粒体膜电位,并诱导了线粒体介导的细胞凋亡。然而,紫锥花苷处理显着减弱了6-OHDA诱导的这些变化。此外,紫锥花苷还可以显着减轻6-OHDA诱导的炎症反应。进一步的研究表明,紫锥花苷可以减少6-OHDA诱导的PC12细胞中ROS的产生。这些结果表明,紫锥花苷抗6-OHDA诱导的神经毒性的潜在机制可能与通过减少ROS产生来减轻线粒体功能障碍和炎症反应有关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号