MELATONIN ALLEVIATES BLEOMYCIN-INDUCED PULMONARY FIBROSIS IN MICE

M H Karimfar, S Rostami, K Haghani, S Bakhtiyari, A Noori-Zadeh

Article ID: 5794
Vol 29, Issue 2, 2015
DOI: https://doi.org/10.54517/jbrha5794
Received: 9 July 2015; Accepted: 9 July 2015; Available online: 9 July 2015; Issue release: 9 July 2015

Abstract

Pulmonary fibrosis occurs as a common end-stage sequela of a number of acute and chronic lung diseases. Eicosanoids exert crucial roles in inflammatory processes pertinent to fibrogenesis induction, however, the role of cyclooxygenase 2 (COX-2) is not fully elucidated in most pulmonary fibrosis related-disorders. Recently, melatonin (MLN) has been introduced as an effective immuno-modulator and anti-oxidant agent. The present study aimed to investigate the effect of MLN on COX-2 expression in idiopathic pulmonary fibrosis (IPF). Animals were divided into five groups, including: 1) saline control, 2) 1% ethanol control, 3) MLN control, 4) bleomycin (BLM), in which mice were injected with BLM (15 mg/kg, i.p.) two times per week for four weeks, and 5) BLM+MLN, in which MLN was given to mice (10 mg/kg, i.p.) 30 minutes prior to BLM injections for four weeks. MLN administration significantly reduced body weight loss (P<0.05), the rate of mortality, edema formation, lung injury, COX-2 expression (P>0.05), interstitial tissue percentage volume (P<0.05), and also increased the alveolar space percentage volume. MLN attenuated the BLM-induced lung injury responses such as collagen accumulation and airway dysfunction in mice. Finally, histological evidence supported the ability of MLN to inhibit COX-2 expression. Thus, it may serve as a novel potential therapeutic agent for IPF.


Keywords

melatonin;pulmonary fibrosis;cyclooxygenase 2;bleomycin


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