Brazilin exerts protective effects against renal ischemia-reperfusion injury by inhibiting the NF-κB signaling pathway

Abstract

Renal ischemia-reperfusion (I/R) injury is associated with high morbidity and mortality as there is currently no available effective therapeutic strategy with which to treat this injury. Thus, the aim of this study was to investigate the potential protective effects of brazilin, a major active component of the Chinese medicine Caesalpinia sappan L., against renal I/R injury in vitro and in vivo. Rats were subjected to removal of the right kidney and I/R injury to the left kidney (ischemia for 45 min followed by reperfusion for 24 h). Treatment with brazilin (30 mg/kg, administered intravenously at 30 min prior to ischemia) led to the reversal of I/R-induced changes in serum creatinine (Scr) and blood urea nitrogen (BUN) levels, and also attenuated the histopathological damage induced by I/R. Furthermore, TUNEL assay revealed that brazilin reduced cell necrosis, and significantly decreased the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in renal tissue. Moreover, HK-2 cells were used in order to elucidate the mechanisms responsible for the protective effects of brazilin. The levels of phosphorylated IκBα and the nuclear translocation of nuclear factor-κB (NF-κB) were all evidently decreased by brazilin. These findings suggested that pre-treatment with brazilin protects against I/R-induced renal damage and suppresses the inflammatory response by inhibiting the activation of the NF-κB signaling pathway.

Up-Regulation of HMGB1 Exacerbates Renal Ischemia-Reperfusion Injury by Stimulating Inflammatory and Immune Responses through the TLR4 Signaling Pathway in Mice

“…Consistent with our study, Jia et al found that 24 h after I/R, the rats developed remarkable renal dysfunction implied by an increase in the BUN and Scr levels [21]. Furthermore, the BUN and Scr levels in the HMGB1 group exceeded those in the I/R group and the levels in the WT mice surpassed those in the TLR44 -/-mice, indicating that HMGB1 and TLR4 contribute to IRI.…”

Retracted: Effects of mTOR/NF‐κB signaling pathway and high thoracic epidural anesthesia on myocardial ischemia‐reperfusion injury via autophagy in rats

“…A recent study revealed that autophagy had both detrimental and beneficial influences on the pathology of myocardial I/R injury (Ma, Wang, Chen, & Cao, ). A large number of evidences have demonstrated that the protective effects against I/R injury via NF‐κB and mTOR pathways (Jia et al, ; Kong et al, ; Zhou, Fang et al, 2015). In addition, a previous research showed that the inhibition of NF‐κB restrained the activity of mTOR (Okamoto et al, ).…”

Protective effect of hydroxysafflor yellow A against acute kidney injury via the TLR4/NF-κB signaling pathway

“…The cells were then incubated in a hypoxic/ischemic chamber at 37 °C for 60 min in a humidified atmosphere of 5% CO 2 and 95% N 2 . Finally, the cells were incubated in culture medium in an incubator with 95% air and 5% CO 2 for an additional 24 h as described previously 37 – 40 . For all experiments, the cells were plated at an appropriate density according to the experimental design and grown for 24 h before treatment.…”