ArticleIranian journal of basic medical sciences2026
Quercetin improves ESAT-6-induced pleural mesothelial cell fibrosis by activating the Nrf2/HO-1 pathway.
Article in Iranian journal of basic medical sciences, 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
Objectives: This study investigated the mechanism by which quercetin suppresses oxidative stress and improves fibrosis in human pleural mesothelial cells (HPMCs) induced by the Mycobacterium tuberculosis-specific antigen early secretory antigen target protein-6 (ESAT-6) by activating the Nrf2/HO-1 signaling pathway, thereby suppressing oxidative stress. Materials and Methods: An in vitro model of ESAT-6-induced HPMC fibrosis was established. The effects of various concentrations of quercetin on HPMCs were assessed using the CCK-8 assay. Markers of oxidative stress, such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH), were assessed. Immunofluorescence was utilized to detect levels of nuclear factor erythroid 2-related factor 2 (Nrf2), and western blot analysis was conducted to evaluate the protein levels of Nrf2, heme oxygenase-1 (HO-1), E-cadherin (E-cad), and α-smooth muscle actin (α-SMA). Results: Quercetin significantly improved ESAT-6-induced HPMC proliferation, reduced the oxidative stress marker MDA, and decreased the fibrosis marker α-SMA levels. It also promoted the translocation of Nrf2 into the nucleus in ESAT-6-induced pleural mesothelial cell fibrosis. Furthermore, quercetin enhanced the enzymatic activity of antioxidants, particularly GSH and SOD, and increased the expression levels of HO-1, Nrf2, and E-cad. Conclusion: The findings indicate that quercetin can inhibit oxidative stress by modulating the Nrf2 pathway and up-regulating HO-1 activity, thereby improving ESAT-6-induced pleural mesothelial cell fibrosis.
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