Stroke is the largest contributor to global neurological disability-adjusted life-years, posing a huge economic and social burden to the world. Though pharmacological recanalization with recombinant tissue plasminogen activator and mechanical thrombectomy have greatly improved the prognosis of patients with ischemic stroke, clinically, there is still no effective treatment for the secondary injury caused by cerebral ischemia. In recent years, more and more evidences show that neuroinflammation plays a pivotal role in the pathogenesis and progression of ischemic cerebral injury. Microglia are brain resident innate immune cells and act the role peripheral macrophages. They play critical roles in mediating neuroinflammation after ischemic stroke. Microglia-mediated neuroinflammation is not an isolated process and has complex relationships with other pathophysiological processes as oxidative/nitrative stress, excitotoxicity, necrosis, apoptosis, pyroptosis, autophagy, and adaptive immune response. Upon activation, microglia differentially express various receptors, channel proteins, and enzymes involved in promoting or inhibiting the inflammatory processes, making them the targets of intervention for ischemic stroke. To inhibit microglia-related neuroinflammation and promote neurological recovery after ischemic stroke, numerous biochemical agents, cellular therapies, and physical methods have been demonstrated to have therapeutic potentials. Though accumulating experimental evidences have demonstrated that targeting microglia is a promising approach in the treatment of ischemic stroke, the clinical progress is slow. Till now, no clinical study could provide convincing evidence that any biochemical or physical therapies could exert neuroprotective effect by specifically targeting microglia following ischemic stroke.

中风是导致全球神经功能障碍调整生命年的最大因素，对世界构成了巨大的经济和社会负担。尽管用重组组织纤溶酶原激活剂和机械血栓切除术进行药理再通已大大改善了缺血性中风患者的预后，但在临床上，仍没有有效的方法治疗因脑缺血引起的继发性损伤。近年来，越来越多的证据表明神经炎症在缺血性脑损伤的发病机制和发展中起着关键作用。小胶质细胞是大脑固有的固有免疫细胞，并起着外周巨噬细胞的作用。它们在介导缺血性中风后在介导神经炎症中起关键作用。小胶质细胞介导的神经炎症不是一个孤立的过程，并且与其他病理生理过程具有复杂的关系，例如氧化/硝化应激，兴奋性毒性，坏死，凋亡，发烧，自噬和适应性免疫反应。激活后，小胶质细胞会差异表达与促进或抑制炎症过程有关的各种受体，通道蛋白和酶，从而使它们成为缺血性中风的干预目标。为了抑制小胶质细胞相关的神经炎症并促进缺血性中风后的神经恢复，已证明许多生化试剂，细胞疗法和物理方法具有治疗潜力。尽管越来越多的实验证据表明，靶向小胶质细胞是治疗缺血性中风的一种有前途的方法，临床进展缓慢。到目前为止，尚无任何临床研究可提供令人信服的证据，表明任何生物化学或物理疗法均可通过在缺血性中风后特异性靶向小胶质细胞来发挥神经保护作用。