Study on the mechanisms of pathogenesis of critical illness polyneuropathy and protective effect of activated factor X.

危重症多发性神经病发病机制及活化因子X的保护作用研究。

• 批准号: 23592687
• 负责人: HINO Hirofumi
• 金额: $ 2.66万
• 依托单位: St. Marianna University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592687/
• 关键词: 敗血症; 重症末梢神経炎; 電位依存性Naチャネルサブタイプ; チャネロパチー; 末梢神経炎; ナトリウムチャネル; glycocalyx; ダナパロイド; アンチトロンビン; 抗凝固薬

We measured the expression of eight kinds of voltage-dependent sodium channel receptor subtypes (Nav) of the sciatic nerve by the real-time PCR method in sepsis induced critical illness polyneuropathy rat model (L-group) and compared to the control group (C-group). We achieved the results shown the significant reductions of gene expression in three subtypes of Nav and increases in three different kinds of Nav in L-group compared to C-group. These data implied the different types of sodium channel gene expression plays an important role in the mechanisms of pathogenesis of critical illness polyneuropathy as channelopathy.Since the administration of Drug-X and/or Drug-Y did not improve the alteration in Nav gene expression, other actions of Drug-X and Drug-Y might be involved in the improvement of nerve function during sepsis.

采用实时荧光定量PCR法检测8种电压依赖性钠通道受体亚型（Nav）在脓毒症致危重症多发性神经病大鼠模型（l组）中的表达，并与对照组（c组）进行比较。我们获得的结果显示，与c组相比，l组Nav的三个亚型的基因表达显著降低，三种不同类型的Nav的基因表达显著增加。这些数据提示不同类型的钠通道基因表达在重症多神经病变作为通道病的发病机制中起重要作用。由于给药药物- x和/或药物- y并没有改善Nav基因表达的改变，因此药物- x和药物- y的其他作用可能参与了脓毒症期间神经功能的改善。