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Chelerythrine-mediated targeting of NF-κB and Nrf2 pathways alleviates liver injury in a carbon tetrachloride-induced liver fibrosis mouse model

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dc.contributor.authorDing Yisong
dc.contributor.authorLi Xiaoming
dc.contributor.authorQi Ruixing
dc.contributor.authorSu Yingshi
dc.contributor.authorWang Xiaoli
dc.contributor.departmentBiología Celular e Histología
dc.date.accessioned2025-10-28T08:36:35Z
dc.date.available2025-10-28T08:36:35Z
dc.date.issued2025
dc.description.abstractBackground and Aims. This study aimed to investigate the mechanism and efficacy of chelerythrine (CHE) in treating carbon tetrachloride (CCl4)-induced liver fibrosis, with a particular focus on the nuclear factor-erythroid-related factor-2 (Nrf2) and nuclear factor-kappa-B (NF-κB) signaling pathways. Methods. Mice were induced with CCl4 for eight weeks and categorized into the control group, CCl4 model group, and CHE low (7 mg/kg/d, ig,), medium (14 mg/kg/d, ig), and high-dose (28 mg/kg/d, ig) groups with 10 animals in each group. Following CHE treatment, liver sample morphology was assessed using multiple immunohistochemistry, and serum biochemical indicators were measured. ELISA was used to determine IL-10, IL-1β, and TNF-α contents. Western blotting and RT-PCR were employed to analyze protein and mRNA levels of α-SMA, Col-I, fibronectin, Nrf2, HO-1, NQO1, GCLc, GCLm, NF-κB, p-NF-κB, IκBα, and p-IκBα. Nrf2 knockout mice were used to assess the impact of CHE on the Nrf2 signaling pathway. Results. The findings demonstrated that CHE significantly ameliorated oxidative damage, inflamma-tory response, and liver fibrosis in CCl4-induced mice. CHE treatment increased Nrf2 expression and its target proteins, including HO-1 and GCLc, an effect not observed in Nrf2 knockout mice. In addition, CHE reduced NF-κB expression levels. Conclusions. These results suggest that CHE can alleviate liver fibrosis in CCl4-induced mice by modulating NF-κB/IκBα and Nrf2 signaling pathways. These findings propose CHE as a potential novel anti-liver fibrosis drug
dc.formatapplication/pdf
dc.format.extent11
dc.identifier.citationHistology and Histopathology, Volúmen 40,nº11(2025), 1805-1815
dc.identifier.doihttps://doi.org/10.14670/HH-18-892
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/169689
dc.languageeng
dc.publisherUniversidad de Murcia, Departamento de Histología e Histopatología
dc.relationQiqihar Medical Sciences Institute Project, Grant/Award Number: QMSI2023Z-05; Graduate Student Innovation Fund Project of Qiqihar Medical University, Grant/Award Number: QYYCX2022-35; Clinical research fund project of Qiqihar Medical Sciences Institute, Grant/Award Number: QMSI2024L-09, QMSI2024L-01
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectChelerythrine
dc.subjectCCl4
dc.subjectLiver fibrosis
dc.subjectNrf2/ NF-κB signaling pathway
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleChelerythrine-mediated targeting of NF-κB and Nrf2 pathways alleviates liver injury in a carbon tetrachloride-induced liver fibrosis mouse model
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.40, Nº11, (2025)