脑创伤(TBI)后血肿形成是引起继发性脑损伤的重要原因，研究发现手术清除血肿预后不良的概率反而高于非手术组，促进机体自身血肿清除成为治疗新策略。小胶质细胞是中枢神经介导血肿清除的主要吞噬系统。我们前期研究发现通窍活血汤能上调CD36表达增强小胶质细胞吞噬能力减小血肿面积，然而其分子机制仍不清楚。本项目拟从确定通窍活血汤进入TBI小鼠颅内吸收成分出发，应用蛋白质组学、分子生物学和液质联用等技术，基于整体、细胞和分子水平三个层次，结合体内（小鼠TBI模型）和体外（小鼠小胶质细胞牵张损伤模型）实验研究，阐明通窍活血汤及其颅内吸收成分通过调控PEBP1/15LO诱导CD36表达激活Mertk/Nr4a1信号促进小胶质细胞对血肿清除；同时比较通窍活血汤和颅内吸收成分促进血肿清除减轻神经损伤的疗效，明确通窍活血汤治疗TBI的颅内药效物质基础，开辟通窍活血汤及其药效物质脑保护作用机制研究的新途径。

Hematoma formation after traumatic brain injury (TBI) is a leading cause of the secondary brain injury. Studies suggested patients with poor prognosis in the surgical clearance group were higher than those in the non-surgical group. Promoting the clearance of hematoma became a new treatment strategy. Microglia are the main phagocytic system in the central nervous system for hematoma clearance. Our previous study found that Tongqiao Huoxue decoction(TQHX) could increase CD36 expression, reduce the hematoma area and promote the recovery of neurological function, but its mechanism is still unclear. This project from determining the composition of the intracranial absorption, uses proteomics, molecular biology and LC-MS technology, bases on the whole, cellular and molecular levels, and combines with (TBI) model in vivo and in vitro (microglia tension damage model) in mice, aims to clarify that TQHX and its absorption through PEBP1/15LO induced CD36 activation regulating MertK/Nr4a1 expression promote hematoma clearance by microglia; At the same time, the effects of TQHX and intracranial absorption components on promoting hematoma clearance and alleviating neuron injury were compared, to clarify the intracranial pharmacodynamic material basis of TQHX on TBI, and open up a new way to study the brain protective mechanism of TQHX.