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<p>Pulmonary fibrosis (PF) is an age onset respiratory disease with no established remedy. Bleomycin (BLM) is a classical anti-cancer drug has been reported to induce inflammation followed by fibrosis in lung and is readily used as an experimental pulmonary fibrosis model. BLM triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release and oxidative stress damages in lung tissues. Thus targeting oxidative stress is a better approach to treat PF. N-Acetyl Cysteine (NAC) is a well-known ROS scavenger. This study examines how NAC abrogates fibrotic development in lung micro-environment by hindering TGF-β/Smad signalling through Nuclear Factor Erythroid 2–related Factor 2 (Nrf2) activation. NAC was found to enhance the expression of Nrf2 and, reduced generation of reactive oxygen species. Suppressed canonical TGF-β/Smad signalling post NAC treatment also observed. NAC mediated Nrf2 activation and TGF-β suppression cumulatively down regulated myofibroblast activation and halted the progression of fibrosis in experimental pulmonary fibrosis. The present study addresses that ROS scavenger mediates hindering of the TGF-β/Smad signalling through Nrf2 activation and reduces fibrosis in lung.</p>

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ROS Scavenger Mediated Modulation of TGF-β/Smad Signalling Through Nrf2 Activation Which Alters the Fibrotic Phenotype in Experimental Pulmonary Fibrosis

  • 期刊论文

  • 发表日期：

    2025年6月18日

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  • Kaustav Chakraborty,
  • Soumya Chatterjee,
  • Arindam Bhattacharyya

摘要

Pulmonary fibrosis (PF) is an age onset respiratory disease with no established remedy. Bleomycin (BLM) is a classical anti-cancer drug has been reported to induce inflammation followed by fibrosis in lung and is readily used as an experimental pulmonary fibrosis model. BLM triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release and oxidative stress damages in lung tissues. Thus targeting oxidative stress is a better approach to treat PF. N-Acetyl Cysteine (NAC) is a well-known ROS scavenger. This study examines how NAC abrogates fibrotic development in lung micro-environment by hindering TGF-β/Smad signalling through Nuclear Factor Erythroid 2–related Factor 2 (Nrf2) activation. NAC was found to enhance the expression of Nrf2 and, reduced generation of reactive oxygen species. Suppressed canonical TGF-β/Smad signalling post NAC treatment also observed. NAC mediated Nrf2 activation and TGF-β suppression cumulatively down regulated myofibroblast activation and halted the progression of fibrosis in experimental pulmonary fibrosis. The present study addresses that ROS scavenger mediates hindering of the TGF-β/Smad signalling through Nrf2 activation and reduces fibrosis in lung.