继发性脑损伤是脑出血（ICH）高死亡率、高致残率的重要原因，研究其发生机制对于ICH的治疗有重要意义。Tenascin-C（TNC）蛋白是一种基质细胞蛋白，在ICH中作用机制尚不清楚。我们预实验发现:重组TNC蛋白能够诱导体外小胶质细胞向M1亚型极化；ICH后早期血肿周围皮层内TNC蛋白明显升高，皮层内小胶质细胞向M1亚型极化；TNC蛋白升高早于toll样受体4(TLR4)及炎性因子。据此，我们提出假说，在ICH发生后，颅内压升高、氧化应激反应等因素刺激血肿周围神经胶质细胞大量分泌TNC蛋白，促进小胶质细胞向M1亚型极化，通过TLR4受体启动损伤相关分子模式通路，引起神经细胞损伤，破坏脑血管屏障，并级联放大ICH后的炎性反应。本研究拟从分子、细胞和整体水平，利用ICH模型、基因敲除小鼠，探讨TNC蛋白在ICH后具体作用机制，并研究以TNC蛋白作为治疗靶点的疗效，为ICH治疗提供新思路。

The secondary brain injury is one of the most important reasons responsible for the high mortality and morbidity after intracerebral hemorrhage (ICH). Thus, it is important to study the mechanism of the secondary brain injury for the treatment of ICH. Tenascin-C protein (TNC) is one of the most important matricellular proteins. However, the detailed mechanism is not well studied in ICH. Our preliminary experimental results indicated that the TNC protein could trigger the polarization of microglia to the M1 phenotype. We also found that TNC protein level around the hematoma increased quickly earlier than toll-like receptor 4 and inflammatory factors. Furthermore, the microglia around the hematoma was found to polarize to M1 phenotype after ICH onset. Thus, we raised the hypothesis: Increased intracranial pressure and oxidative stress response after ICH up-regulated TNC protein which was subsequently cleaved by matrix metalloproteinases（MMPs） or other proteinase. The TNC protein modulates the adhesion, mobility and polarization of microglia cells. The cleaved TNC (cl-TNC) protein initiated the damage-associated molecular pattern signal pathway and aggravated the inflammatory response through the toll-like receptor 4 (TLR4) and the up-regulated MMP-9 expression which damaged the neuroglia cells and destroyed the BBB. To verify this hypothesis, we apply the mice ICH model in vivo and cultured microglia in vitro, and use methods of western blot, immunofluorescence and genetic knockout technology. From the molecular, cellular and body levels, we explore the role and detailed mechanism of TNC protein and the possible treatment targeting at TNC in the secondary brain injury after intracerebral hemorrhage.