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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。
OBJECTIVE: To investigate the effect of baicalin on TLRs-NOD2 receptor in cerebral ischemia and pneumonia model and to explore the common mechanism of inflammatory lesion in lung and brain. Methods: The models of cerebral ischemia-reperfusion and acute pneumonia in mice were established. After intraperitoneal injection of baicalin, the expression of TLR2 / 4, NOD2 and TNFα in mouse brain and lung tissue were detected. Results: The expression of TLR2 / 4, NOD2 and TNFα were significantly higher in the brain and lung tissues of mice with brain injury. Baicalin could down-regulate these factors to some extent. In the brain tissues and lung tissues of mice with pneumonia, the expressions of TLR2 / 4, NOD2 and TNFα were highly expressed to varying degrees, baicalin could inhibit these factors to varying degrees. CONCLUSION: Baicalin has a significant regulatory effect on TLR2 / 4, NOD2 receptor and downstream inflammatory cytokines TNFα. The regulatory effect and its effect on inflammatory response may be the common basis of its effects on lung and brain lesions.