Effect of Trichostatin A on Bleomycin Induced Pulmonary Fibrosis in Mice and its Mechanism
Department of Respiratory and Critical Care Medicine, The First Central Hospital Affiliated to Nankai University, 1Department of Respiratory and Critical Care Medicine, Tianjin Medical University General Hospital, Heping, Tianjin 300052, 2Department of General Education Courses, Cangzhou Medical College, Yunhe, Hebei 061000, China
Qian Zhang, Department of Respiratory and Critical Care Medicine, The First Central Hospital Affiliated to Nankai University, Tianjin 300052, China, E-mail: firstname.lastname@example.org
To investigate the effect and mechanism of trichostatin A on bleomycin induced pulmonary fibrosis in mice compared with dexamethasone and pirfenidone is the objective of the study. C57 black 6 mice were instilled intranasal bleomycin to establish pulmonary fibrosis model. They were divided into five groups: Control group, model group, dexamethasone group, pirfenidone group and trichostatin A group. Hematoxylin and eosin staining and Masson’s staining was conducted; the expression of related proteins in each group was observed by immunohistochemistry and Western blotting. Hematoxylin and eosin staining and Masson’s staining showed that the lung tissue was damaged in varying degrees, interstitial protein deposition, basal cell hyperplasia and a large number of macrophage infiltration in the alveolar cavity. The lung tissue injury in trichostatin A group was the least. The expression of vimentin, collagen-I, alpha smooth muscle actin and other interstitial proteins in the model group increased significantly, and the expression of above interstitial proteins in each intervention treatment group decreased in varying degrees, especially in trichostatin A group. The expression of suppressor of mothers against decapentaplegic homolog 7 protein decreased significantly in the model group and increased significantly in the trichostatin A group; there was no significant difference in the expression of p38-mitogen-activated protein kinase protein in each group. The expression of interstitial protein messenger RNA such as vimentin, collagen-I and alpha smooth muscle actin peaked on the 14th d after modeling. Trichostatin A could significantly inhibit the progression of pulmonary fibrosis by inhibiting the activity of histone deacetylase 1, while histone deacetylase 1 could activate transforming growth factor beta-1/suppressor of mothers against decapentaplegic pathway, involved in the progression of pulmonary fibrosis. Dexamethasone could not delay or improve pulmonary fibrosis, or even aggravate the progression of pulmonary fibrosis.