1,3-β-葡聚糖可激活自噬诱发小鼠肺组织炎症

1,3-β-Glucan can activate autophagy and induce lung tissue inflammation in mice

目的探讨1,3-β-葡聚糖诱导炎症小鼠的肺组织自噬水平,为肺组织炎症的预防、诊断及治疗提供依据。方法将20只实验小鼠分为两组,1,3-β-葡聚糖实验组、生理盐水对照组,每组10只。小鼠非暴露气管灌注1,3-β-葡聚糖,于灌注后第3天、第28天分别收集小鼠肺组织。采用苏木素伊红和Masson染色,观察肺组织病理改变;采用Western blot检测小鼠体内自噬特异性蛋白微管相关蛋白1轻链3(LC3)和自噬相关蛋白sequestosome 1(p62)的表达水平。结果镜下可见,与对照组相比,实验组小鼠肺组织出现大量炎症细胞和胶原沉积。Western blot结果显示,实验组小鼠体内LC3-Ⅱ表达水平较对照组升高(t=-2.932,P<0.05),p62表达水平较对照组升高(t=-5.151,P<0.05)。结论1,3-β-葡聚糖可明显著提高小鼠肺组织自噬特异性蛋白LC3及自噬相关蛋白p62的表达水平,证明肺组织炎症的小鼠细胞自噬水平升高。

Objective To study the autophagy level of lung tissue in mice with pulmonary inflammation induced by perfusion of 1,3-β-Glucan.Methods Twenty experimental mice were divided into two groups,1,3-β-Glucan experimental group and normal saline control group,with 10 mice in each group.Non exposed tracheal perfusion of 1,3-β-Glucan in mice,the lung tissues of mice were collected on the 3rd and 28th day after perfusion.H&E and Masson staining were used to observe the pathological changes of lung tissue;Western blot was used to detect the expression levels of autophagy specific proteins microtubule associated protein 1 light chain 3(LC3)and autophagy related proteins sequestosome 1(p62)in mice.Results Microscopically,compared with the control group,a large number of inflammatory cells and collagen deposition appeared in the lung tissue of the experimental group.Western blot showed that the expression levels of LC3-Ⅱin the experimental group was higher than that in the control group(t=-2.932,P<0.05),and the expression levels of p62 was higher than that in the control group(t=-5.151,P<0.05).Conclusion 1,3-β-Glucan can significantly upregulate the expression levels of autophagy specific proteins LC3 and autophagy related proteins p62 in mice's lung tissue,indicating that the levels of autophagy in mice with lung tissue inflammation increase.