巨噬细胞作为先天性免疫反应的主要效应细胞，在调节蛛网膜下腔出血早期炎症反应中起到重要作用。先前研究发现在不同病理微环境下，巨噬细胞能极化为M1促炎型和M2抑炎型。我们前期研究发现与脑缺血性卒中相反，巨噬细胞在蛛网膜下腔出血早期以M1型为主，加重炎症反应。采用RNA array检测发现PI3Kγ、STAT6及NF-κB在调节巨噬细胞极化过程中起到重要作用。据此我们提出以下假说：外周巨噬细胞在SAH早期浸润至损伤脑组织并极化为M1型，释放促炎因子加重早期炎症反应，PI3Kγ能够通过磷酸化STAT6和抑制NF-κB表达从而促进巨噬细胞从M1型转化为M2型，从而降低NLRP3炎症小体的表达，减轻早期脑损伤。本课题拟从分子、细胞、组织以及动物水平等多个维度阐明巨噬细胞极化在蛛网膜下腔出血早期炎症反应中的作用及机制。本研究的开展有望为蛛网膜下腔出血的治疗提供新的靶点。

Macrophages, as the main effector cells of innate immune response, play an important role in regulating the early-stage inflammation of subarachnoid hemorrhage (SAH). Previous studies have indicated that macrophages can be polarized to pro-inflammatory type M1 and anti-inflammatory type M2 under different pathological microenvironments. Our previous study showed that M1 macrophages predominate in the early stages of SAH, which aggravates the inflammatory response. RNA array detection found that PI3Kγ, STAT6, and NF-κB play an important role in the regulation of macrophage polarization. Therefore, we propose the following hypothesis: Peripheral macrophages infiltrated into injured brain tissues in the early stage of SAH and polarized into type M1, releasing proinflammatory cytokines and aggravating the early-stage inflammatory response. PI3Kγ can convert macrophages from type M1 to type M2 through phosphorylating STAT6 and inhibiting NF-κB, thus reducing the expression of the NLRP3 inflammasome and alleviating early brain injury. Our study intends to clarify the role and mechanism of macrophage polarization in the early-stage inflammatory response of subarachnoid hemorrhage from multiple dimensions such as molecular, cell, tissue and animal level. Our study is expected to provide a new target for the treatment of subarachnoid hemorrhage.