ArticleHistology and histopathology2026
Targeting thrombin with hirudin alleviates paraquat-induced pulmonary fibrosis via the PAR-1-mediated TGF-β1 pathway.
Article in Histology and histopathology, 2026. 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
backgroundParaquat (PQ)-induced pulmonary fibrosis (PF) is a serious disease without specific antidotes. Thrombin is important for promoting fibrosis development. We aimed to explore whether thrombin promotes PQ-induced PF by activating the protease-activated receptor-1 (PAR-1)-mediated transforming growth factor-β1 (TGF-β1) pathway.
methodsMale Sprague Dawley rats received PQ treatment, either alone or with thrombin or hirudin (a thrombin inhibitor) (n=9 in the control, model, thrombin, and hirudin groups). After 7 or 14 days of treatment, oxidative stress (OS) indicators and histopathological damage in the lungs were detected. PF degree was evaluated using Masson staining and hydroxyproline levels in lung tissues and collagen levels in bronchoalveolar lavage fluid. Furthermore, type I collagen (Col-1), TGF-β1, and PAR-1 expression, as well as extracellular signal-regulated kinase 1/2 (ERK1/2) and mothers against decapentaplegic homolog 3 (Smad3) phosphorylation in the lungs, were assessed. To investigate the mechanism of thrombin on PQ-induced PF, rats treated with PQ and thrombin further received SCH79797 (a PAR-1 inhibitor) alone or combined with SRI-011381 (a TGF-β agonist) (n=9 in the thrombin+SCH79797 and thrombin+SCH79797+SRI-011381 groups). In addition to Masson staining and detection of the above-mentioned genes and proteins, alpha-smooth muscle actin (α-SMA), TGFβ receptor type I (TβRI), and type II (TβRII) expression in the lungs were also detected.
resultsBoth 7 and 14 days of thrombin treatment triggered OS, exacerbated lung histopathological damage, and promoted PF in PQ-stimulated rats. Furthermore, thrombin upregulated Col-1, TGF-β1, and PAR-1 expression as well as ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats. However, hirudin produced the opposite results. Additionally, the role of thrombin in promoting PF, increasing Col-1, TGF-β1, α-SMA, PAR-1, TβRI, and TβRII expression and ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats was reversed by SCH79797, while the inhibitory effects of SCH79797 were counteracted by SRI-011381.
conclusionsThrombin may promote PQ-induced PF by activating PAR-1-mediated TGF-β1, suggesting that PAR-1-mediated TGF-β1 is a potential target for preventing PQ-induced PF.
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