Protective effect of rutin against bleomycin induced lung fibrosis: Involvement of TGF‐β1/α‐SMA/Col I and III pathway

• Published in: BioFactors (Oxford) Vol. 46; no. 4; pp. 637 - 644
• Main Authors: Bai, Linlin, Li, Aimin, Gong, Cuike, Ning, Xuecong, Wang, Zhihua
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01-07-2020
• Subjects: bleomycin; lung fibrosis; rutin; TGF‐β1; α‐SMA; bleomycin; α-SMA; TGF-β1; rutin; lung fibrosis
• ISSN: 0951-6433; 1872-8081
• DOI: 10.1002/biof.1629

Lung fibrosis is a progressive fatal lung disorder with significantly high mortality rates. Bleomycin (BLM) is one of the most commonly used chemotherapeutic agents for the treatment of several carcinomas. The most severe adverse effect of BLM is lung toxicity; therefore, BLM has been repeatedly reported to be considered amongst the most widely used agents for the induction of experimental lung fibrosis. In the current study, rutin has been investigated for its ability to ameliorate BLM‐induced pulmonary fibrosis. BLM was instilled intratracheally and rutin was administered orally (50 and 100 mg/kg) for 3 weeks. Rutin significantly decreased lung/body weight index, bronchoalveolar lavage fluid lactate dehydrogenase activity, total cell count, macrophages, and lymphocyte counts. Rutin significantly decreased lung malondialdehyde content, increased lung glutathione content, superoxide dismutase activity, serum total antioxidant capacity, and decreased lung nitric oxide content. Moreover, rutin reduced expressions of transforming growth factor beta 1 and other fibrosis‐related biomarkers (Col I, Col III, and α‐SMA). In addition, rutin significantly ameliorated histological changes and prevented collagen deposition with the paralleled decrease in lung hydroxyproline content. In conclusion, rutin can be proposed to be a potential therapeutic agent for the management of lung fibrosis.