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

由巨噬细胞浸润到周围神经损伤部位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性质。因此，我们使用未部分坐骨神经结扎（PSNL）小鼠模型研究了巨噬细胞介导的PPARγ信号在外周炎症触发的神经病理性疼痛中的作用。在神经病理性疼痛的早期阶段，通过调节炎症部位的巨噬细胞浸润和促炎分子的产生，PPARγ治疗显著减轻了触觉异常性疼痛的发展。我们的研究结果表明，在早期阶段激活巨噬细胞中的PPARγ信号可能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.