Tannic acid alleviates experimental pulmonary fibrosis in mice by inhibiting inflammatory response and fibrotic

Nandhine Rajasekar1, Ayyanar Sivanantham1, Amrita Kar2

  • 1Department of Biotechnology, BIT-Campus, Anna University, Tiruchirappalli, Tamil Nadu, 620024, India.

Insights

Tannic acid (TA), a natural polyphenol, shows promise in treating pulmonary fibrosis (PF). TA significantly reduced lung scarring, inflammation, and fibrosis markers in a mouse model, suggesting potential clinical applications for PF treatment.

Area of Science:

  • Pulmonology
  • Pharmacology
  • Natural Products Chemistry

Background:

  • Pulmonary fibrosis (PF) is a progressive lung disease characterized by irreversible scarring.
  • Limited effective therapeutic options exist for PF, necessitating the exploration of novel treatments.

Purpose of the Study:

  • To investigate the therapeutic potential of tannic acid (TA), a dietary polyphenol, in a bleomycin (BLM)-induced mouse model of pulmonary fibrosis.
  • To evaluate the effects of TA on histological alterations, inflammatory responses, and fibrotic processes in the lungs.

Main Methods:

  • Pulmonary fibrosis was induced in mice via intratracheal administration of bleomycin (BLM).
  • Mice were treated with tannic acid (TA) to assess its impact on PF.
  • Histological analysis, inflammatory mediator quantification, and assessment of pro-fibrotic and fibrotic marker expression were performed.
  • The effect of TA on Erk1/2 phosphorylation in lung tissue was examined.

Main Results:

  • TA administration significantly attenuated BLM-induced lung histological damage and inflammatory cell infiltration.
  • TA treatment reduced the levels of inflammatory mediators, including nitric oxide, leukotriene B4, and cytokines.
  • TA suppressed the expression of pro-fibrotic markers such as transforming growth factor-β1, alpha-smooth muscle actin, vimentin, collagen 1 alpha, and fibronectin.
  • TA inhibited BLM-induced phosphorylation of Erk1/2 (extracellular signal-regulated kinases 1 and 2) in the lungs.

Conclusions:

  • Tannic acid demonstrates significant potential to mitigate pulmonary fibrosis by inhibiting inflammatory and fibrotic pathways.
  • TA's ability to reduce lung scarring and associated molecular markers suggests its utility as a therapeutic agent for PF.
  • These findings support the further investigation of tannic acid for clinical application in treating pulmonary fibrosis.

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