小胶质细胞介导的炎性反应参与脑缺血再灌注损伤的研究进展
Chinese Journal of Geriatric Heart Brain and Vessel Diseases（2019）
Abstract
缺血性脑卒中严重危害人类健康,具有高发病率、高致残率、高死亡率等特点,其中老年患者居多[1].临床上,积极溶栓是其主要治疗手段,但若血栓自溶或溶栓药物使用超过时间窗,血流再通后可引起脑缺血再灌注损伤,脑缺血再灌注损伤发病机制复杂,其中级联炎性反应是其主要病理过程之一[2-3].小胶质细胞作为脑内常驻免疫细胞,在受到损伤刺激后迅速激活,吞噬病原体,进行组织修复,但过度激活则释放大量的促炎因子及神经毒性物质,导致炎性反应级联放大,参与脑缺血再灌注损伤.近期研究表明,衰老与急性应激源如缺血再灌注损害程度具有相关性,衰老的小胶质细胞免疫监视和吞噬能力下降,且在损伤和有害刺激下更易产生大量促炎因子,介导持续炎性反应,加重脑损伤[4].干预小胶质细胞过度激活或阻止其释放神经毒性代谢物,抑制炎症级联反应,可能是脑缺血再灌注损伤治疗的潜在靶点.本研究将对近几年相关文献进行梳理总结,为上述作用机制及靶点提供有力理论依据.
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