Neuroprotective effects of PPARγon ischemic neuronal injury

合成过氧化物酶体增殖物激活受体γ(PPARγ)配体，噻唑烷二酮，用于治疗2型糖尿病。此外，它们还具有多效性，如对缺血性神经元损伤的神经保护作用；然而，其神经保护作用的机制尚不清楚。在本研究中，我们检测了短暂性前脑缺血后ppar γ的表达，并评估了噻唑烷二酮对该模型的神经保护作用。我们还研究了噻唑烷二酮类药物对缺血后促存活信号通路Akt/ gsk -3β和STAT3的影响。我们发现ppar γ主要在缺血后的神经元中上调，噻唑烷二酮通过激活Akt/ gsk -3β和stat3通路对缺血性神经元损伤具有神经保护作用。

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.