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Thy-1 depletion and integrin β3 upregulation-mediated PI3K-Akt-mTOR pathway activation inhibits lung fibroblast autophagy in lipopolysaccharide-induced pulmonary fibrosis

机译:Thy-1耗竭和整联蛋白β3上调介导的PI3K-Akt-mTOR途径激活抑制脂多糖诱导的肺纤维化中的肺成纤维细胞自噬。

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摘要

LPS-induced autophagy inhibition is accompanied with Thy-1 downregulation and integrin β3 upregulation in LPS-induced pulmonary fibrosis. The severity of pulmonary fibrosis was determined by hematoxylin-eosin (H&E) staining; collagen deposition was revealed by MASSON staining (magnification, ×200) ( ). The expression of α-SMA in lung tissues was also measured by Western blot ( ). Collagen deposition was measured by hydroxyproline content and collagen level assessments ( ). Representative Western blot images showing expression of Thy-1, integrin β3, LC3 and P62 in the lung tissue ( ). Values are mean ± SD (  = 6). *  P
机译:LPS诱导的肺纤维化中,LPS诱导的自噬抑制作用伴随Thy-1下调和整联蛋白β3上调。肺纤维化的严重程度由苏木精-伊红(H&E)染色确定。 MASSON染色显示胶原沉积(放大倍数,×200)()。肺组织中α-SMA的表达也通过蛋白质印迹法()测定。胶原蛋白沉积通过羟脯氨酸含量和胶原蛋白水平评估()进行测量。代表性的Western印迹图像显示Thy-1,整联蛋白β3,LC3和P62在肺组织中的表达()。值是平均值±SD((= 6)。 * P

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