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Mechanism of Xuebijing Injection in ameliorating sepsis-induced acute kidney injury by regulating TLR4/MyD88/NF-κB signaling pathway in rats
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DOI   10.11656/j.issn.1672-1519.2025.08.16
Key Words   Xuebijing Injection;sepsis;acute kidney injury;TLR4/MyD88/NF-κB signaling pathway
Author NameAffiliationE-mail
LI Jinkui Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
ZHANG Junfei Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
DU Wujun Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
YANG Lishan Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
MA Lei Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China  
MA Xiao Emergency Department, General Hospital of Ningxia Medical University, Yinchuan 750000, China maxiaoxiao008@163.com 
Abstract
    [Objective] To investigate the protective mechanism of Xuebijing Injection(XBJ) against sepsis-induced acute kidney injury through TLR4/MyD88/NF-κB signaling pathway in rats. [Methods] Eighteen SD rats were randomly divided into Sham operation group,model group and Xuebijing group,with 6 rats in each group. The renal index was calculated,and the pathological changes of renal tissue were determined by hematoxylin-eosin(HE) staining. The expression levels of creatinine(Cr),blood urea nitrogen(BUN),neutrophil gelatinase associated lipocalin(NGAL),kidney injury molecule-1(Kim-1),tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) were detected by ELISA kits. The expression levels of TLR4,MyD88,p-NF-κB,Bcl-2,Bax and Cleaved Caspase 3 were detected by Western blot. [Results] Compared with the model group,the Xuebijing group could effectively reduce the expression levels of Cr,BUN,NGAL,Kim-1,TNF-α and IL-6,and the difference was statistically significant(P<0.05). At the same time,the Xuebijing group reduced the degree of pathological injury and renal index in the rats with sepsis-induced acute kidney injury. At the same time,compared with the model group,XBJ treatment could significantly reduce the expression levels of Bax and Cleaved Caspase 3,and increase the expression level of Bcl-2 protein,the difference was statistically significant(P<0.05). In addition,XBJ treatment significantly reduced the protein expression levels of TLR4,MyD88 and p-NF-κB compared with model group(P<0.05). [Conclusion] XBJ continuous treatment can reduce the degree of sepsis-induced acute kidney injury and improve renal function,and its mechanism may be related to the inhibition of TLR4/MyD88/NF-κB signaling pathway to reduce inflammatory response and apoptosis.

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