黄芩苷对哮喘大鼠气道重塑作用的实验研究

目的: 初步探讨黄芩苷对支气管哮喘气道重塑的防治作用及其作用机制。方法: 用卵清白蛋白（OVA）致敏大鼠制备支气管哮喘气道重塑动物模型，经黄芩苷干预治疗，用免疫组化法检测各组大鼠肺组织匀浆中α-平滑肌肌动蛋白（α-SMA）、磷酸化细胞外信号调节激酶1/2（p-ERK1/2）及气道组织中转化生长因子-β1（TGF-β1）蛋白的表达量；用RT-PCR检测气道平滑肌（ASM）中p-ERK1/2的mRNA水平。结果: 实验结果显示，p-ERK1/2、α-SMA、TGF-β1蛋白的表达量在模型组中有明显的增加，地塞米松组、黄芩苷高剂量组和低剂量组的p-ERK1/2、α-SMA、TGF-β1蛋白的表达量均低于模型组（P<0.05，P<0.01）。结论: 黄芩苷可降低TGF-β1、α-SMA的蛋白表达，并影响ERK信号传导通路，下调p-ERK1/2 mRNA含量，从而减轻气道炎症，延缓气道重塑。

Effect of baicalin on airway remodeling of bronchial asthma

AIM: To explore the effect and mechanism of baicalin on the airway remodeling of bronchial asthma. METHODS: Animal models of airway remodeling in asthmatic rats were induced by egg albumen (OVA). After the treatment of Baicalin, expressions of TGF-β1, p-ERK1/2 and α-SMA in the lung tissue of rats were detected by immunohistochemical method, and the level of p-ERK1/2 mRNA in the airway smooth muscle (ASM) was detected by RT-PCR. RESULTS:Expressions of p-ERK1/2, α-SMA and TGF-β1 were significantly increased in the model group, which were all higher than those of dexamethasone group, baicalin high dose group and low dose group (P<0.05 or P<0.01). CONCLUSION: Baicalin can decrease the expression of TGF-β1, α-SMA, affect the ERK signal pathways, down regulate the content of p-ERK1/2 mRNA , thereby reducing airway inflammation and delaying airway remodeling.