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Brazilin attenuates kidney ischemia- reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction

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dc.contributor.authorLulu Zhang
dc.contributor.authorFei Mu
dc.contributor.authorYing Yu
dc.contributor.authorChen Cui
dc.contributor.authorMeng Tang
dc.contributor.authorKexin Sun
dc.contributor.authorYanping Yin
dc.contributor.authorJingwen Wang
dc.contributor.authorRui Gong
dc.contributor.authorJinyi Zhao
dc.contributor.departmentBiología Celular e Histología
dc.contributor.editorUniversidad de Murcia, Departamento de Biología Celular e Histología
dc.date.accessioned2026-03-25T17:04:41Z
dc.date.available2026-03-25T17:04:41Z
dc.date.issued2026
dc.description.abstractBrazilin, a natural homoisoflavonoid, is the primary bioactive ingredient derived from the bark and heartwood of Caesalpinia sappan L. It has been proven to exhibit multiple biological activities and therapeutic potential in chronic degenerative diseases, fibrotic disorders, inflammatory diseases, and cancers. However, whether it is involved in regulating the pathological process of acute kidney injury (AKI) is not fully understood. This study aimed to elucidate the role and key pharmacological molecular mechanisms of brazilin in AKI. Our data demonstrated that pretreatment with brazilin can significantly reduce the high expression of serum creatinine (Scr), blood urea nitrogen (BUN), and lipocalin-2 (LCN2) in mice exposed to ischemia/ reperfusion (I/R) and alleviate kidney histopathological damage. Meanwhile, pretreatment with brazilin can alleviate apoptosis, inflammation, and oxidative stress injury in the kidney tissue cells by partially inhibiting the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammatory pathway or activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase‐1 (HO-1) antioxidant pathway. In vitro, pretreatment with brazilin significantly downregulated pro-apoptotic Bax and upregulated anti apoptotic Bcl-2 expression in human renal proximal tubular cells (HK-2) subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). Besides, it ameliorated mitochondrial dysfunction by enhancing mitochondrial biogenesis and restoring mitochondrial membrane potential. These effects collectively suppressed oxidative stress injury and NLRP3 inflammasome signaling pathway activation. In summary, brazilin exhibits significant protective effects against I/R-induced AKI by attenuating inflammation, oxidative stress and cell apoptosis, and mitochondrial damage. These findings suggest that brazilin holds promise as a potential therapeutic agent for AKI.
dc.formatapplication/pdf
dc.format.extent17
dc.identifier.doihttps://doi.org/10.14670/HH-18-982
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/223121
dc.languageeng
dc.relationSin financiacion externa a la Universidad
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.subjectKidney ischemia-reperfusion injury
dc.subjectInflammation
dc.subjectOxidative stress
dc.subjectMitochondrial damage
dc.subjectBrazilin
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleBrazilin attenuates kidney ischemia- reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.41, Nº4, (2026)