摘要
目的探讨转化生长因子(TGF-β1)通过调节磷脂酰肌醇3-激酶(PI3K)分子影响肺纤维化进程的重要机制。方法应用博来霉素构建KM鼠肺纤维化模型,设置联合TGF-β1+SB-431542组、单纯TGF-β1组、联合TGF-β1+LY294002组、对照亚组、空白组,于建模后3、7、14、28d检测各组羟脯氨酸(HYP)含量;应用免疫组化技术检测各组磷脂酰肌醇3-激酶(PI3K)蛋白表达;应用方差分析法比较各组PI3K表达差别。结果相对空白组,实验各组PI3K明显高表达,主要分布在细胞核外;单纯TGF-β1组,PI3K及羟脯氨酸(HYP)含量明显高于其余联合TGF-β1+LY294002组。结论 PI3K可能参与TGF-β1调节肺纤维化过程的机制,抑制PI3K的表达,可能可以阻碍肺纤维化疾病发展。
Objective The study aim is to elucidate the mechanism and function of TGFβ1 and PI3K in pulmonary fibrosis. Methods Construct mouse pulmonary fibrosis model via BLM,Set TGF-β1＋SB-431542,TGF-β1,TGF-β1＋LY294002,black,the control groups respectively.After build model,at 3,7,14,28d,detect HYP content in every groups.Analyses PI3K expression via IHC,and the difference by χ^2.Results compared to blank group,in all experiment groups,the expression of PI3K was significant higher（P0.05）;at TGF-β1group,the content of PI3K,HYP were significant higher than TGF-β1＋LY294002 group.Conclusion PI3K may take part in the mechanism of TGF-β1 in pulmonary fibrosis progression.Down-regulate PI3K expression may inhibit the progression of pulmonary fibrosis.
出处
《咸宁学院学报（医学版）》
2012年第4期286-288,共3页
Journal of Xianning Univarsity(medical Sciences)
