Abstract
This study aimed to investigate the effect and mechanism of tranilast (TR) on bleomycin (BLM) induced pulmonary fibrosis in a rat model, pulmonary fibrosis was induced in rats by using intratracheal bleomycin and the serum and lungs were collected 28 days later. The serum levels of IL-4 and IFN-γ were determined by ELISA and IL-4/IFN-γ was calculated. Reverse transcription polymerase chain reaction (RT-PCR) was employed to measure the mRNA expression of TGF-β1. Immunohistochemistry was employed to detect the protein expression of TGF-β1 followed by evaluation of alveolitis and fibrosis. When compared with BLM group and glucocorticoid (GC) group, the INF-γ level was markedly increased and IL-4 level dramatically decreased in the TR group with a significant decrease of IL-4/INF-γ ratio. The mean optical density and mRNA expression of TGF-β1 were markedly decreased accompanied by low scores of alveolitis and fibrosis. Significant differences were observed between TR groups (medium and high dose) and BLM group as well as control group (P < 0.05) in the aforementioned parameters. Moreover, marked difference was also observed among TR groups (P < 0.05) in the aforementioned parameters. Both TR and GC can affect the Th1/Th2 lymphocyte balance and inhibit the TGF-β1 expression improving the BLM induced pulmonary fibrosis. Key words: Th1/Th2, tranilast, pulmonary fibrosis, interferon-γ, transforming growth factor-β1.
Highlights
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease, with a median survival of 3 to 5 years (Barqaqli et al, 2009)
Increased IL-4 level was noted in the medium dose tranilast group when compared with high dose tranilast group (P = 0.001).The same tendency was seen at IL4/IFN
It was used as an antiallergic drug and can inhibit the degranulation of mast cells and basophils, which suppresses the release of mediators involving in the anaphylaxis including histamine and 5-HT
Summary
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease, with a median survival of 3 to 5 years (Barqaqli et al, 2009). Oxidative stress with reactive oxygen species (ROS) plays an important role in the process of pulmonary fibrosis (Barqaqli et al, 2009). Excessive levels of reactive oxygen species (ROS) may damage cellular macromolecules. Macrophages are integrated into all stages of the fibrotic process, perhaps because they serve as key regulators of fibroblast recruitment, proliferation and activation. They promote fibrosis by secreting chemokines and specific matrix metalloproteinases that degrade extracellular matrix (ECM) components, facilitating the recruitment of inflammatory cells to sites of tissue injury (Wynn, 2011)
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