神经炎症的持续存在和神经损伤修复滞后是神经病理性疼痛维持的核心因素。我们认为，巨噬细胞和小胶质细胞具有抗炎和促修复的双重潜能，如果通过损伤微环境中的关键分子激活固有免疫细胞，就可能作为治疗神经病理性疼痛的新策略。本研究不再从抑制NF-κB和NLRP3炎症小体等常规抗炎机制出发，而是尝试利用AMPK作为分子开关，激活巨噬细胞和小胶质细胞上的Gas6-MerTK受体系统，一方面通过MerTK受体诱发SOCS3高表达来抑制神经炎症；另一方面激活MerTK受体提升胞葬作用并利用胞葬完成以后释放的IL-10和TGF-β等物质，主动诱发炎症消退和神经修复。本研究有助于阐明胞葬效应和SOCS3上调在神经病理性疼痛控制中的分子机制和关键作用，也为后续临床治疗方案和药物开发提供新的思路和治疗靶标。

The persistence of nerve inflammation and the delay in the repair of nerve damage are two core factors for the maintenance of neurological pain. We believe that macrophages and microglias have the dual potential to inhibit inflammation and to promote regeneration. Therefore, activating intrinsic macrophages by key molecules in the microenvironment may be a new strategy for the treatment of neuropathic pain. In this study, instead, we attempt to use AMPK as a molecular switch to activate the Gas6-MerTK receptor system on macrophages and microglias. First, high expression of SOCS3 might be induced by MerTK receptor to inhibit nerve inflammation; second, activating MerTK receptors might promote efferocytosis and IL-10 / TGF-β release to induce inflammation regression and nerve regeneration. Our study may help to elucidate the molecular mechanism and key role of efferocytosis and SOCS3 upregulation in the control of neuropathic pain, and to provide new targets for clinical treatment and drug development.