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Home > Archives > Volume 20, No 8 (2022) > Article

DOI: 10.14704/nq.2022.20.8.NQ44953

Montelukast effect on Clara Cell secretory protein (CC16) and Krebs von den Lungen6(KL-6)in pulmonary fibrosis rats model

Mohammed rabahmahdi1 , Dr. Gaithalijasim, Dr. Wassan Abdul Kareem Abbas

Abstract

Pulmonary fibrosis(PF) is a condition in which the lungs became scarred and breathing becomes difficult. The most common type is idiopathic pulmonary fibrosis (IPF) which occurred to an unknown cause.PF pathogenesis passes through three stages the first one is an injury of alveolar cells followed by the inflammation stage then the repair stage. Bleomycin causes pulmonary fibrosis due to a lack of deactivating enzymes bleomycin hydrolase. Administration of bleomycinintratracheally causes injury of alveolar cells type II causing the release of inflammatory markers such as Interleukins (as IL-4) and transforming growth factor beta(TGFβ1) which cause conversion of fibroblast to myofibroblast that finally leads to fibrosis. Pirfenidone is an antifibrotic agent, that has anti-inflammatory and antioxidant effects by inhibition of TGFβ1. Montelukast is Cysteinyl leukotrienes (CysLT) antagonist bind to corresponding CysLT receptors like CysLT type-1 receptors located on respiratory airway smooth muscle cells, airway macrophages, and on various pro-inflammatory cells like eosinophils and some specific myeloid stem cells activities causing anti-inflammatory effect by inhibition of inflammatory markers as TGFβ1. In this study, we investigate the impact and mechanisms of montelukast on the pulmonary fibrosis rats model. Rats were divided into five groups, the control group received distilled water by gastric gavage for 28 days, the induction group received bleomycinintratracheally as a single dose, pirfenidone group received pirfenidone 50mg/kg for 28 days after 14 days from bleomycin dose, montelukast group was received montelukast 20mg/kg for 28 days after 14 days from bleomycin dose and the combination group received a half dose of pirfenidone and montelukast for 28 days after 14 days of bleomycin dose. After twenty-eight days from the treatment with montelukast or pirfenidone sacrifice rats and collect the blood samples from each group and compare the results by measuring the biomarkers [cub cell secretory protein 16 (CC16), Krebs von den lungen-6 (KL-6), platelet-derived growth factor (PDGF), IL-4 and TGFβ1]. We observed that the induction group elevated the level of all these markers after 14 days from bleomycin dose but pirfenidone, montelukast, and combination decreased the level of these markers after 28 days of treatment. In conclusion,montelukast has anti-inflammatory and antifibrotic effects by decreasing the level of inflammatory markers and TGFβ1 which is a key cytokine responsible for pulmonary fibrosis.

Keywords

Pulmonary fibrosis(PF) is a condition in which the lungs became scarred and breathing becomes difficult

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