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Published:
Nov 16, 2020DOI:
10.4314/tjpr.v19i7.5Keywords:
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Main Article Content
Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway
Abstract
Purpose: To investigate the therapeutic effect of loureirin B (LB) on amiodarone (AD)-induced pulmonary fibrosis (PF).
Methods: Forty-eight male C57BL/6 mice, 8–10 weeks of age, were divided into four groups (n=12). Oral administration of amiodarone hydrochloride (AD) was performed for 4 weeks to induce pulmonary fibrosis. The degree of fibrosis was assessed by Masson staining, while collagen I and α-smooth muscle actin (α-SMA) levels were evaluated by Western blot analysis. ELISA was used to measure the levels of cytokines TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) and lung tissue. Levels of p- Smad2, Smad2, p-Smad3 and Smad3 were determined by western blotting.
Results: AD treatment increased the collagen levels and expression levels of collagen I and α-smooth muscle actin (α-SMA) in lung tissue and of inflammatory cytokines TNF-α, IL-1β, and IL-6, in both bronchoalveolar lavage fluid (BALF) and lung tissue in a dose-dependent manner (p < 0.01).
Furthermore, AD increased the levels of p-Smad2/3. AD-induced increases in collagen I and α-SMA levels were reversed by loureirin B (LB). In addition, LB reduced AD-induced increased levels of the inflammatory cytokines TNF-α, IL-1β, and IL-6 in both bronchoalveolar lavage fluid (BALF) and lung tissue (p < 0.01).
Conclusion: These results demonstrate that LB downregulates expression of fibrosis-related proteins and suppresses AD-induced PF. The mechanism responsible for the protective effect of LB on ADinduced PF might involve inhibition of the Smad2/3 pathway. Thus, LB is a potential therapeutic agent for the management of PF.
Keywords: Amiodarone, Loureirin B, Pulmonary fibrosis, Smad, Inflammation
