脑出血已成为影响全球公共健康的重要问题。ICH后激活的小胶质/巨噬细胞可极化为M1和M2两种亚型。糖尿病加重ICH脑损伤可能与高血糖增加脑组织内活性氧簇,促使小胶质/巨噬细胞向M1促炎亚型趋化有关。脂联素受体(Adiponectin receptor，AdipoRs)在脑组织细胞中广泛分布，具有抗糖尿病、抗炎等多种功能。基于先前的研究报道和预实验结果，我们推测AdipoR1受体激活很可能降低糖尿病ICH后血肿周围组织活性氧簇水平，抑制由其引起的NF-kB入核，进而抑制小胶质向M1状态极化。AdipoR1受体激活亦能协同转录调节因子STAT6促使小胶质/巨噬细胞向M2状态极化。除小胶质细胞外，AdipoR1受体可直接降低神经元内活性氧簇水平，减轻线粒体损伤，最终发挥“双重”脑保护作用。更为重要的是，我们旨在利用搜集的临床ICH患者脑组织标本进一步验证该通路在临床范围的有效性。

Intracerebral hemorrhage (ICH) has become an important issue affecting global public health. The microglia/macrophages can be activated and polarized into two subtypes (M1 and M2) after ICH. The potential mechanism that hyperglycemia aggravates ICH-induced brain injury may be that hyperglycemia increases reactive oxygen species (ROS) which promotes the M1 proinflammatory subtype polarization in brain tissue . Adiponectin receptor (AdipoRs) is widely distributed in brain tissue cells and has many functions such as anti-diabetes and anti-inflammatory. According to previous studies and the pilots results, we hypothesized that AdipoR1 receptor activation may reduce ROS levels in the perihematomal tissue after ICH, inhibit ROS-induced NF-kB nucleation and M1 state polarization. AdipoR1 receptor activation also synergizes with the transcriptional regulator STAT6 to promote the M2 state polarization. In addition to microglia, AdipoR1 receptor can directly reduce ROS levels and reduce mitochondrial damage in neurons, and ultimately exert dual functions in neuroprotection. More importantly, we aimed to validate the clinical effectivity of AdipoR1 receptor by using the collected brain tissue samples from clinical ICH patients. At the same time, RNA sequence technology was used to explore the changes of gene transcription level of hyperglycemia around the hematoma, and to explore the potential signaling pathways affecting the microglia/macrophage polarization, which provides a new target for the treatment of secondary brain injury after ICH.