Silibinin alleviates silica-induced pulmonary fibrosis: Potential role in modulating inflammation and epithelial-mesenchymal transition.

Pulmonary fibrosis (PF) is a devastating interstitial lung disease resulting from indefinite causes with very few limited, those too ineffective therapeutic options. Earlier evidence reported inflammation and epithelial-mesenchymal transition (EMT) are the major threats in PF. The present study was aimed to examine the anti-fibrotic activity of silibinin (SB) in PF. PF was induced by administering oropharyngeal 1.5 mg/mice silica on day 1, followed by treatment with and without oral SB for 14 days. Lung injury was assessed by x-ray analysis on day 14 and all the animals were sacrificed on day 15. The results showed that silica remarkably altered the histoarchitecture and induced the expression of inflammatory components in BALF and pulmonary tissue. Immunoblotting investigation quantified the expression of TGF-β, p-smad2/3, collagen-I, fibronectin, and α-SMA in the pulmonary tissue. To this end, treatment with SB alleviated inflammatory components, including IL-1β, IL-6, and TNF-α in the fibrotic tissue. Moreover, SB harnessed the tissue architecture, improved diffusive scattering of x-ray signals, and modulated epithelial-mesenchymal phenotypic alterations, including TGF-β, p-smad2/3, and collagen-I. Altogether, the significant reduction of inflammatory signaling, collagen deposition, and epithelial-mesenchymal transdifferentiation by SB suggested that it could be used as a potential therapeutic candidate to treat pulmonary inflammation and fibrosis.