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Troxerutin Protects Kidney Tissue against BDE-47-Induced Inflammatory Damage
through CXCR4-TXNIP/NLRP3 Signaling
#MMPMID29849929
Shan Q
; Zheng GH
; Han XR
; Wen X
; Wang S
; Li MQ
; Zhuang J
; Zhang ZF
; Hu B
; Zhang Y
; Zheng YL
Oxid Med Cell Longev
2018[]; 2018
(?): 9865495
PMID29849929
show ga
2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) induces oxidative stress in kidney
cells, but the underlying mechanism remains poorly understood. Troxerutin, a
natural flavonoid, has potential antioxidant and anti-inflammatory efficacy. In
this study, we assessed the effect of troxerutin on kidney damage caused by
BDE-47 and investigated the underlying mechanism. The results showed troxerutin
reduced reactive oxygen species (ROS) level and urine albumin-to-creatinine ratio
(ACR), decreased the activities of inflammatory factors including
cyclooxygenase-2 (COX-2), induced nitric oxide synthase (iNOS) and nuclear factor
kappa B (NF-?B) in the kidney tissues of BDE-47-treated mice. Furthermore,
troxerutin significantly weakened the expression of kidney NLRP3 inflammasome
containing NLRP3, ASC, and caspase-1, contributing to the decline of IL-1?.
Additionally, troxerutin inhibited the increased protein level of stromal-derived
factor-1(SDF-1), C-X-C chemokine ligand 12 receptor 4 (CXCR4), and thioredoxin
interaction protein (TXNIP) caused by BDE-47. Specifically, the
immunoprecipitation assay indicated that there was a direct interaction between
CXCR4 and TXNIP. CXCR4 siRNA and TXNIP siRNA also decreased the inflammatory
damage, which was similar to the action of troxerutin. Our data demonstrated that
troxerutin regulated the inflammatory lesions via CXCR4-TXNIP/NLRP3 inflammasome
in the kidney of mice induced by BDE-47.
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