目的：通过研究黄芩苷对脑缺血和肺炎模型中TLRs-NOD2受体的影响，探讨肺、脑相关炎性病变的共同机制。方法：分别建立小鼠脑缺血再灌和急性肺炎模型，造模后对小鼠腹腔注射黄芩苷，检测小鼠脑和肺组织中TLR2/4、NOD2和TNFα蛋白的表达。结果：脑损伤模型小鼠脑组织和肺组织中，TLR2/4、NOD2和TNFα显著高表达，黄芩苷能够不同程度的下调这些因子；肺炎模型小鼠脑组织和肺组织中，TLR2/4、NOD2和TNFα不同程度的高表达，黄芩苷可以在不同程度上抑制这些因子。结论：黄芩苷对TLR2/4、NOD2受体及下游炎性因子TNFα存在着显著的调控作用，这种调控作用及对炎性反应的影响可能是其对肺、脑病变作用的共同基础。

This study was aimed to investigate the regulation effect of baicalin on TLRs-NOD2 in cerebral ischemia model and pneumonia model in order to discuss the common pathological mechanism of both models. The cerebral ischemia reperfusion mice model and acute pneumonia mice model were established. Baicalin was intraperitoneal injected into the mice. Then, protein expressions of TLR2/4, NOD2 and TNFα in the brain and lung tissues were detected. The results showed that protein expressions of TLR2/4, NOD2 and TNFα were significantly upregulated in the brain and lung tissues of brain injury model. And baicalin is able to downregulate these factors at different levels. Protein expressions of TLR2/4, NOD2 and TNFα were increased significantly at different levels in the brain and lung tissues of the pneumonia model. Baicalin is able to inhibit these factors at different levels. It is concluded that baicalin has obvious regulation effect on TLR2/4, NOD2 and downstream inflammatory factor TNFα. This regulation effect and inflammatory mechanism may be the common basis of baicalin effect in the treatment of lung and brain diseases.

国家自然科学基金项目(30973896)：从黄芩苷对TLRs-NOD2模式识别及相关信号转导通路的调控探讨肺、脑相关炎性病变的共有机制，负责人：邢东明；科学技术部国家“重大新药创制”科技重大专项（2009ZX09502）：与药效相关的中药质量评价关键技术研究，子课题负责人：杜力军；科学技术部国家“重大新药创制”科技重大专项（2009ZX09308-003-33）：中药生产技术及过程控制技术标准平台，子课题负责人：雷帆。