Tannic acid alleviates experimental pulmonary fibrosis in mice by inhibiting inflammatory response and fibrotic process
- PDF / 2,728,141 Bytes
- 14 Pages / 595.276 x 790.866 pts Page_size
- 23 Downloads / 172 Views
Inflammopharmacology
ORIGINAL ARTICLE
Tannic acid alleviates experimental pulmonary fibrosis in mice by inhibiting inflammatory response and fibrotic process Nandhine Rajasekar1 · Ayyanar Sivanantham1 · Amrita Kar2 · Santanu Kar Mahapatra2 · Rajesh Ahirwar4 · Rajesh K. Thimmulappa3 · Sudhakar Gandhi Paramasivam1 · Rajasekaran Subbiah1,4 Received: 16 January 2020 / Accepted: 9 April 2020 © Springer Nature Switzerland AG 2020
Abstract Pulmonary fibrosis (PF) is a chronic and irreversible scarring disease in the lung with limited treatment options. Therefore, it is critical to identify new therapeutic options. This study was undertaken to identify the effects of tannic acid (TA), a naturally occurring dietary polyphenol, in a mouse model of PF. Bleomycin (BLM) was intratracheally administered to induce PF. Administration of TA significantly reduced BLM-induced histological alterations, inflammatory cell infiltration and the levels of various inflammatory mediators (nitric oxide, leukotriene B4 and cytokines). Additionally, treatment with TA also impaired BLM-mediated increases in pro-fibrotic (transforming growth factor-β1) and fibrotic markers (alpha-smooth muscle actin, vimentin, collagen 1 alpha and fibronectin) expression. Further investigation indicated that BLM-induced phosphorylation of Erk1/2 (extracellular signal-regulated kinases 1 and 2) in lungs was suppressed by TA treatment. Findings of this study suggest that TA has the potential to mitigate PF through inhibiting the inflammatory response and fibrotic process in lungs and that TA might be useful for the treatment of PF in clinical practice. Keywords Tannic acid · Natural compound · Bleomycin · Transforming growth factor-β · Inflammation · Pulmonary fibrosis
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10787-020-00707-5) contains supplementary material, which is available to authorized users. * Sudhakar Gandhi Paramasivam [email protected] * Rajasekaran Subbiah [email protected] 1
Department of Biotechnology, BIT‑Campus, Anna University, Tiruchirappalli, Tamil Nadu 620024, India
2
Centre for Research in Infectious Diseases (CRID), School of Chemical and Biotechnology, SASTRA Deemed to be University, Thanjavur, Tamil Nadu 613401, India
3
Department of Biochemistry, JSS Medical College, JSS Academy of Higher Education and Research, Mysore, Karnataka 570015, India
4
Department of Biochemistry, ICMR-National Institute for Research in Environmental Health, Bhopal, Madhya Pradesh 462030, India
Progressive tissue fibrosis is a common pathological response of organs with several known and/or unknown causes, which is associated with higher morbidity and mortality rates (Kekevian et al. 2014). In the lung, the fibrosis is characterized by alveolar inflammation, redox imbalance, inflammatory injury to the alveolar epithelium, subsequent deregulation of epithelial–fibroblastic interactions, aberrant proliferation of fibroblasts, excessive accumulation of extra
Data Loading...
