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目的:观察平喘宁对寒性哮喘大鼠肺组织中转化生长因子-β1(TGF-β1)、细胞周期蛋白D1(Cyclin D1)和磷酸化细胞外信号调节激酶1、2(p-ERK1/2)m RNA表达的影响。方法:雄性SD大鼠105只,随机分为正常组、模型组、桂龙咳喘宁组、地塞米松组、平喘宁高剂量组、平喘宁中剂量组、平喘宁低剂量组,每组15只。以卵蛋白致敏及寒冷刺激复制大鼠哮喘模型,造模21d后,正常组、模型组每天给予蒸馏水灌服,其它各组给予相应药物灌服,4周后解剖大鼠并取出肺组织。采用免疫组化法测定肺组织中TGF-β1、Cyclin D1的含量,采用RT-PCR检测平喘宁治疗哮喘前后p-ERK1/2 m RNA表达的变化。结果:和正常组比较,模型组发生明显炎性细胞侵润,气道平滑肌增厚;肺组织TGF-β1、Cyclin D1的表达水平上升(P<0.05,P<0.01);p-ERK1/2 m RNA表达水平提高(P<0.05,P<0.01)。和模型组比较,各治疗组肺组织病理改变有不同程度的好转;TGF-β1、Cyclin D1表达下降,p-ERK1/2 m RNA表达水平降低(P<0.05,P<0.01)。结论:平喘宁可通过抑制P-ERK1/2 m RNA表达,调节ERK信号转导通路,抑制TGF-β1、Cyclin D1表达,抑制气道重塑而治疗哮喘。
Objective: To observe the effect of Pingchuanning on the expression of TGF-β1, Cyclin D1 and p-ERK1 / 2) m RNA expression. Methods: 105 male SD rats were randomly divided into normal group, model group, Guilong Kechuanning group, dexamethasone group, Pingchuanning high dose group, Pingchuanning middle dose group, Pingchuanning low dose group , Each group of 15. The asthma model was induced by ovalbumin sensitization and cold stimulation. After 21 days of modeling, the normal group and the model group were given distilled water every day. The other groups were given the corresponding drugs. Four weeks later, the rats were dissected and the lung tissue was taken out. The contents of TGF-β1 and Cyclin D1 in lung tissue were determined by immunohistochemical method. The expression of p-ERK1 / 2 mRNA in asthmatic rats was detected by RT-PCR. Results: Compared with normal group, inflammatory cell infiltration and thickening of airway smooth muscle were observed in model group. The expression of TGF-β1 and Cyclin D1 in lung tissue was increased (P <0.05, P <0.01), and the expression of p-ERK1 / 2 m RNA expression increased (P <0.05, P <0.01). Compared with the model group, the pathological changes of the lung tissue in each treatment group improved to some extent; the expression of TGF-β1 and Cyclin D1 decreased and the expression of p-ERK1 / 2 m RNA decreased (P <0.05, P <0.01). Conclusion: Pingchuanning can treat asthma by inhibiting the expression of P-ERK1 / 2mRNA, regulating ERK signal transduction pathway, inhibiting the expression of TGF-β1 and Cyclin D1 and inhibiting airway remodeling.