...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Degenerative Neurological and Neuromuscular Disease >Effect of the micro-immunotherapy medicine 2LPARK? on rat primary dopaminergic neurons after 6-OHDA injury: oxidative stress and survival evaluation in an in vitro model of Parkinson’s disease
【24h】

Effect of the micro-immunotherapy medicine 2LPARK? on rat primary dopaminergic neurons after 6-OHDA injury: oxidative stress and survival evaluation in an in vitro model of Parkinson’s disease

机译：微量免疫治疗药2LPARK的作用？对6-OHDA损伤后大鼠原代多巴胺能神经元的影响：帕金森氏病体外模型中的氧化应激和存活评估

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background: Parkinson’s disease (PD) is a neurodegenerative disease characterized by motor impairments and resulting from progressive degenerative loss of midbrain dopaminergic (DAergic) neurons in the substantia nigra. Although the main cause of the loss of DAergic neurons is still unknown, various etiopathogenic mechanisms are distinguished, including release and accumulation of endogenous excitotoxic mediators along with the production of oxidative free radicals. Several neurotrophic and growth factors are known to increase DAergic neuronal survival and enhance antioxidant mechanisms. In this context, the micro-immunotherapy (MI) approach consists to regulate the immune system in order to protect DAergic neurons and control oxidative stress. Purpose: The aim of the present study was to investigate the effect of the MI medicine (MIM), 2LPARKsup?,/sup (Labo’Life), on oxidative stress and on the number of neurons positive for tyrosine hydroxylase (TH), in an in vitro model of PD. Methods: Rat primary mesencephalic DAergic neurons cultures were pre-treated for 1 hr with the MIM (10 μM and 10 mM), placebo (10 μM and 10 mM) or brain-derived neurotrophic factor (BDNF; 3.3 μM) and then intoxicated with 6-hydroxydopamine (6-OHDA; 20 μM) for 48 hrs. After incubation, cells were incubated 30 mins at 37°C with CellROX green reagent and number of labeled cells were quantified. Then, cells were fixed and incubated with anti-TH antibody and the number of THsup+,/sup neurons was evaluated. Results: We showed that, contrary to placebo, MIM was able to reduce oxidative stress and protect DAergic neurons from 6-OHDA-induced cell death. Conclusion: Our results demonstrate the in vitro efficacy of MIM on two essential mechanisms of PD and propose the MI approach as a new ally in the regulation of neuroinflammation and in the treatment of this degenerative disease.
机译：背景：帕金森氏病（PD）是一种神经退行性疾病，其特征是运动障碍，是由黑质中脑多巴胺能（DAergic）神经元进行性退化引起的。尽管DAergic神经元丧失的主要原因尚不清楚，但各种致病机理已被区分，包括内源性兴奋毒性介质的释放和积累以及氧化自由基的产生。已知几种神经营养和生长因子可增加DA能神经元的存活并增强抗氧化机制。在这种情况下，微免疫疗法（MI）的方法包括调节免疫系统，以保护DA能神经元并控制氧化应激。目的：本研究的目的是研究MI药物（MIM），2LPARK ？，（Labo'Life）对氧化应激和酪氨酸羟化酶阳性神经元数量的影响（TH），在PD的体外模型中。方法：用MIM（10μM和10 mM），安慰剂（10μM和10 mM）或脑源性神经营养因子（BDNF; 3.3μM）对大鼠原发性中脑DA能神经元培养物进行1小时预处理，然后中毒6-羟基多巴胺（6-OHDA; 20μM）持续48小时。孵育后，将细胞与CellROX绿色试剂在37°C孵育30分钟，并定量标记的细胞数。然后，将细胞固定并与抗TH抗体一起孵育，并评估TH +，神经元的数量。结果：我们表明，与安慰剂相反，MIM能够减少氧化应激并保护DAergic神经元免于6-OHDA诱导的细胞死亡。结论：我们的结果证明了MIM对PD的两种基本机制的体外疗效，并提出了MI方法作为调节神经炎症和治疗这种退行性疾病的新盟友。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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