Gefitinib Inhibits Bleomycin-Induced Pulmonary Fibrosis via Alleviating the Oxidative Damage in Mice

Figure 4

HMGB34367 was involved in direct regulation of α-SMA expression and was highly expressed in the lung tissues affected by pulmonary fibrosis. Lung tissues were collected 2 weeks after bleomycin (BLM) administration. Pulmonary nuclei were extracted from BLM- or PBS-treated lung tissue. (a) A DNA-nuclear protein pulldown method was used to detect the binding of nuclear proteins to the α-smooth muscle actin (α-SMA) promoter. A 20 kDa protein (HMGB34367) enlarged its binding amount with an α-SMA promoter under BLM conditions. (b) The mRNA expressions of α-SMA and HMGB34367 were increased in lung homogenates after BLM exposure.

(a)

(b)