Neuroprotective effects of PPARγon ischemic neuronal injury

PPARγ对缺血性神经元损伤的神经保护作用

• 批准号: 21591835
• 负责人: KINOUCHI Hiroyuki
• 金额: $ 3万
• 依托单位: University of Yamanashi
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21591835/
• 关键词: PPARγ; 脳虚血; アポトーシス; Akt

Synthetic peroxisome proliferator-activated receptorγ(PPARγ) ligands, thiazolidinediones, are used for the treatment of type 2diabetes. In addition, they have pleiotropic effects such as neuroprotective effects against ischemic neuronal injury ; however, the mechanism of neuroprotective effects is still obscure. In this study, we examined the expression of PPARγafter transient forebrain ischemia, and assessed the neuroprotective effects of thiazolidinediones in this model. We also studied the effects of thiazolidinediones on Akt/GSK-3βand STAT3, key pathways of prosurvival signaling after ischemia. We revealed that PPARγis upregulated mainly in neurons after ischemia, and thiazolidinediones have a neuroprotective effects against ischemic neuronal injury via activation of Akt/GSK-3βand STAT3pathways.

合成的过氧化物酶体增殖物激活受体γ（PPARγ）配体噻唑烷二酮类药物还用于治疗2型糖尿病，此外，它们还具有多种作用，例如针对缺血性神经元损伤的神经保护作用，但其神经保护作用的机制仍不清楚。在这项研究中，我们检测了短暂前脑缺血后 PPARγ 的表达，并评估了噻唑烷二酮类药物的神经保护作用。我们还研究了噻唑烷二酮类药物对缺血后促存活信号传导的关键通路 Akt/GSK-3β 和 STAT3 的影响，我们发现 PPARγ 主要在缺血后的神经元中上调，并且噻唑烷二酮类药物通过激活 PPARγ 对缺血性神经元损伤具有神经保护作用。 Akt/GSK-3β 和 STAT3 通路。