IL-27通过PI3K/Akt通路对哮喘小鼠气道重塑的影响

Effect of IL-27 on airway remodeling in asthmatic mice via PI3K/Akt pathway

目的探究IL-27对哮喘小鼠气道重塑模型的作用,其机制是否与PI3K/Akt信号通路相关。方法18只雌性BALB/c小鼠随机分成3组,即对照组、哮喘组、IL-27治疗组。HE染色法检查小鼠肺组织病理学变化;Masson染色观察小鼠肺组织胶原沉积变化;免疫组织化学法、实时荧光PCR及Western blot检测肺组织中α-SMA的表达水平;Western blot对肺组织中Akt的磷酸化水平进行定量分析。结果IL-27治疗能明显减轻哮喘小鼠气道炎症和气道壁厚度。此外,IL-27能减轻哮喘小鼠气道胶原沉积和α-SMA的表达。Western blot结果显示,IL-27抑制p-Akt的蛋白表达量。结论IL-27通过PI3K/Akt通路减轻哮喘小鼠气道重塑。

Aim To explore the effect of IL-27 on airway remodeling in asthmatic mice and whether the mechanism is related to PI3K/Akt signaling pathway.Methods Eighteen female BALB/c mice were randomly divided into three groups,namely control group,OVA group and IL-27 treatment group.The histopathological changes of lung in mice were detected by HE staining.The changes of collagen deposition in lung tissues of mice were observed by Masson staining.The expression of alpha-smooth muscle actin(α-SMA)in lung tissues was detected by immunohistochemistry,real-time PCR and Western blot.The phosphorylation of Akt in lung tissues was assessed by Western blot.Results IL-27 treatment significantly reduced airway inflammation and airway wall thickness in asthmatic mice.In addition,IL-27 reduced airway collagen deposition andα-SMA expression in asthmatic mice.Western blot results showed that IL-27 inhibited p-Akt protein expression.Conclusion IL-27 alleviates airway remodeling in asthmatic mice through the PI3K/Akt pathway.