Effect of Thalidomide on Cox-2 expression in bleomycin-induced pulmonary fibrosis in mice

Abstract

Introduction: Lung fibrosis is a progressive, fatal disease that is characterized by increasing fibroblasts proliferation and extracellular matrix precipitation. Studies have shown that cyclooxygenase- 2 (Cox-2) could play a crucial role in the pathogenesis of lung fibrosis. In the current study, the effect of thalidomide on bleomycin-induced pulmonary fibrosis was qualitatively studied in a laboratory animal model. \nMethods: Thirty-two adult male C57BL/6 mice were randomly assigned to the following four groups: Group one received 2 mg bleomycin, group two received bleomycin in addition to 4 mg of thalidomide; group three received 4 mg of thalidomide, and Group 4 received 0.1 mg of 0.5% carboxymethyl cellulose (CMC) via intraperitoneal (IP) administration. Finally, the expression of Cox-2 protein and the percentage of contact points of alveolar spaces and pulmonary connective tissue were determined. \nResults: Our results showed that in the Bleo + Thal group compared to the Bleo group, the percentage of contact points of pulmonary connective tissue decreased significantly (P<0.001), while the percentage of contact points among the alveolar spaces increased significantly (P = 0.01). Also, immunohistochemical studies have demonstrated the number of Cox-2+ cells in the volume unit in the Bleo + Thal group decreased significantly in comparison with the group that received only Bleo (P = 0.012). \nConclusion: In conclusion, these results suggest thalidomide could alleviate the bleomycin-induced lung fibrosis and decreases the expression of Cox-2 protein.