ArticleJournal of thoracic disease2025
Effect of pirfenidone on pulmonary fibrosis in acute lung injury via the regulation of the miR-34a-5p/TGF-β1/SMAD pathway.
Article in Journal of thoracic disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Pulmonary fibrosis (PF) is a common phenomenon in acute lung injury (ALI), and miR-34a-5p plays a significant role in injury-like illness. This study aims to investigate the molecular regulatory mechanisms of miR-34a-5p and pirfenidone (PFD) in the pathological process of PF, providing novel experimental data to elucidate the molecular mechanisms underlying the therapeutic effects of miR-34a-5p and PFD in the treatment of PF. Methods: In mouse alveolar macrophage (MH-S) cells, quantitative polymerase chain reaction (qPCR) was employed to assess miR-34a-5p expression. Western blotting was used to examine the protein levels of TGF-β1, p-SMAD3, p-SMAD4, CD68, CD206, Arg-1, and YM-1. Cell Counting Kit-8 (CCK8) assays were conducted to asses cell viability. Animal models were established in male C57BL/6 mice, and lung tissues were obtained for histological analyses. Immunohistochemistry (IHC) was performed to measure the expression of CD206 and YM-1. Results: In IL4-treated MH-S cells, the expression of miR-34a-5p was significantly upregulated according to qPCR, and miR-34a-5p inhibition could improve the cell viability. Western blot data showed that when induced by IL4, the levels of CD68, CD206, Arg-1, and YM-1 were significantly decreased, and miR-34a-5p was also suppressed. M2 macrophage polarization was mediated by miR-34a-5p. Furthermore, after treatment with PFD in IL4-treated MH-S cells, cell viability was increased, which was reversed when miR-34a-5p expression was elevated. Protein expression of CD68, CD206, Arg-1, and YM-1 was significantly reduced. With IL4 treatment, the protein levels of TGF-β1, p-SMAD2, and p-SMAD3 were significantly increased but then decreased when PFD was added. Conclusions: PFD could influence ALI by regulating miR-34a-5p through the TGF-β1/SMAD pathway, which suggests miR-34a-5p as a therapeutic target for ALI treatment.
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