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目的:研究黄芩苷调节哮喘模型小鼠Th1/Th2反应的分子机制。方法:将BALB/c小鼠随机分为6组,分别为正常对照组、模型组、地塞米松阳性对照组及黄芩苷高、中、低剂量组。采用卵蛋白(OVA)腹腔注射致敏与雾化吸入激发法复制哮喘模型,末次激发24 h后处死小鼠,取脾,制备单核细胞悬液,以OVA刺激,培养3 d后取培养上清,应用ELISA法检测其中干扰素γ(IFN-γ)、白细胞介素4(IL-4)、白细胞介素5(IL-5)及白细胞介素10(IL-10)的含量;脾细胞培养2 d后用逆转录PCR(RT-PCR)检测T-bet、GATA-3及STAT-6的表达。结果:黄芩苷能显著抑制IL-4、IL-5的蛋白表达及GATA-3、STAT-6的基因表达;并能提高IL-10的蛋白表达。结论:黄芩苷在体内可能主要通过GATA-3、信号转导和转录激活因子6(STAT-6)等转录因子及IL-10调节Th2反应。
Objective: To study the molecular mechanism of baicalin in regulating Th1 / Th2 response in asthmatic mice. Methods: BALB / c mice were randomly divided into 6 groups: normal control group, model group, dexamethasone positive control group and baicalin high, medium and low dose groups. The asthma model was induced by intraperitoneal injection of ovalbumin (OVA) and atomization inhalation. The mice were sacrificed 24 hours after the last challenge, and the spleen was taken. The mononuclear cell suspension was prepared and stimulated with OVA. After cultured for 3 days, The contents of IFN-γ, IL-4, IL-5 and IL-10 were detected by ELISA. After cultured for 2 days, the expression of T-bet, GATA-3 and STAT-6 were detected by RT-PCR. Results: Baicalin could significantly inhibit the expression of IL-4, IL-5 and GATA-3, STAT-6 gene and increase the protein expression of IL-10. CONCLUSION: Baicalin may regulate Th2 response mainly through transcription factors such as GATA-3, signal transducer and activator of transcription 6 (STAT-6) and IL-10 in vivo.