Publication: Brazilin attenuates kidney ischemia- reperfusion injury by regulating inflammation, oxidative stress, and mitochondrial dysfunction
Authors
Lulu Zhang ; Fei Mu ; Ying Yu ; Chen Cui ; Meng Tang ; Kexin Sun ; Yanping Yin ; Jingwen Wang ; Rui Gong ; Jinyi Zhao
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Publisher
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Universidad de Murcia, Departamento de Biología Celular e Histología
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DOI
https://doi.org/10.14670/HH-18-982
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info:eu-repo/semantics/article
Description
Abstract
Brazilin, 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.
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