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. 2020 Mar 6;12(5):4322–4336. doi: 10.18632/aging.102882

Figure 2.

Figure 2

lncRNA sirt1 antisense (AS) alleviates bleomycin (BLM)-induced pulmonary fibrosis. (A) The expression of sirt1 AS in the pulmonary tissues from control mice or bleomycin (BLM) treated mice that treated with adenovirus sirt1 AS and ad-NC (n=10 per group). (B) H&E and Masson’s trichrome staining showed pulmonary injury and collagen deposition of pulmonary tissues in mice with or without sirt1 AS overexpression. (C) Immunofluorescence staining showing the overlap of E-cadherin (red) and a-SMA (green) in pulmonary tissues with or without sirt1 AS overexpression. (D) Immunohistochemistry analysis indicated the accumulation of collagen 1 and fibronectin 1 in the lung with or without sirt1 AS overexpression. (E–H) QPCR analysis demonstrated the expression of epithelial-mesenchymal transition (EMT)-related markers, α-SMA, E-cadherin, Collagen 1 and Fibronectin1 mRNA in indicated groups (n=10 per group). (I) Western blot showed the relative expression of EMT related markers α-SMA, E-cadherin, collagen1 and fibronectin1 from mice with or without overexpression of sirt1 AS up bleomycin (BLM) treatment; and densitometry quantified data of above indicated markers, represented as a fold change to β-actin. * P<0.05 vs. control group; # P<0.05 vs. BLM+ad-NC group.