脑卒中是国内外首位致死致残原因，幸存者中大都遗留有永久性神经功能障碍，这种神经功能障碍跟免疫性炎症反应介导的中枢神经损伤有关，目前缺乏有效的治疗手段。我们的研究思路是应用小分子介质比如MicroRNA和Sj16，这些小分子能够在血脑屏障没有完全开放的时候顺利地通过,并对卒中后的脑组织发挥免疫调节作用。我们前期研究发现Sj16能抑制脑卒中继发的免疫炎症反应，但其机制不清楚，为进一步临床转化应用，本课题设计：（1）使用miR-155基因敲除的小鼠制作MCAO模型，研究miR-155基因敲除能否有效抑制γδT细胞分泌IL-17，从而减轻脑卒中后的继发性炎症反应（2）通过对脑卒中后的小鼠腹腔注射小分子免疫调节性蛋白Sj16，探索Sj16 能否将脑卒中后Th1促炎反应向Th2的抑炎反应转变（3）探索MicroRNA和小分子蛋白Sj16在改善脑卒中后继发性炎症反应方面是否具有协同作用。

Stroke is the leading cause of the death and disability world-wide, and there is no effective treatment to improve functional recovery in the postischemic phase, mainly due to the secondary brain injury caused by immunopathogenetic inflammation. Our research purpose is to develop novel anti-inflammation therapeutic strategies, such as using small molecule agent miRNAs and sj16 peptide, to let these therapeutic agents efficiently penetrate into the brain parenchyma and make specific function. Our previous study found that intraperitoneal injection of Sj16 after MCAO surgery could inhibit ischemic stroke-induced inflammation, but the underlying mechanism is not clear. For the further clinical translation and application, we design the experimental program: (1) Determine role of miR-155 in suppressing IL-17, including IL-17-producing T cells, in post-ischemic stroke-induced inflammation; (2) Determine effect of altering Th1/Th2 immune response conducted modulation in post-ischemic Stroke-induced inflammation via a peptide sj16;(3) Determine the synergistic effect of MicroRNA and sj16 in reduction of post-ischemic stroke-induced inflammation. The results of this study will open up a new way for the treatment of stroke.