PPARγ agonist rosiglitazone attenuates the development of neuropathic pain by regulating macrophage activation.

巨噬细胞渗入周围神经损伤部位所引发的神经炎症可导致神经病理性疼痛。过氧化物酶体增殖物激活受体γ(PPARγ)信号调节巨噬细胞的特性。因此，我们采用非部分坐骨神经结扎小鼠模型，研究了巨噬细胞介导的PPARγ信号在周围炎症引发的神经病理性疼痛中的作用。神经病理性疼痛早期的PPARγ治疗通过调节炎症部位巨噬细胞的浸润和促炎分子的产生，显着减轻触觉异常痛觉的发展。我们的结果表明，早期激活巨噬细胞中的PPARγ信号可能会抑制神经病理性疼痛的发展。

Neuroinflammation triggered by macrophage infiltration into sites of peripheral nerve injury may result in neuropathic pain. Peroxisome proliferator-activated receptor gamma(PPARγ) signaling regulates the properties of macrophages. So we investigated the macrophage-mediated effects of PPARγ signaling on neuropathic pain triggered by peripheral inflammation using have not been partial sciatic nerve ligation (PSNL) mice model. PPARγ treatment in the early phase of neuropathic pain significantly alleviated the development of tactile allodynia by regulating macrophage infiltration and production of proinflammatory molecules at the inflamed site. Our results indicate that the activation of PPARγ signaling in macrophages during the early phase may suppress neuropathic pain development.