The protein kinase 2 inhibitor tetrabromobenzotriazole protects against renal ischemia reperfusion injury

摘要: Protein kinase 2 (CK2) activation was reported to enhance reactive oxygen species production and activate the nuclear factor κB (NF-κB) pathway. Because oxidative stress inflammation are critical events for tissue destruction during ischemia reperfusion (I/R), we sought determine whether CK2 important in renal response I/R. Mice underwent 25 min of were then reperfused. We confirmed an increased expression CK2α period, while CK2β remained consistent. administered tetrabromobenzotriazole (TBBt), a selective inhibitor before inducing I/R injury. subjected injury showed typical patterns acute kidney injury; blood urea nitrogen serum creatinine levels, tubular necrosis apoptosis, inflammatory cell infiltration proinflammatory cytokine markedly when compared sham mice. However, pretreatment with TBBt abolished these changes improved function architecture. Similar renoprotective effects inhibition observed emodin. Renoprotective associated suppression NF-κB mitogen activated protein (MAPK) pathways. Taken together, results suggest that mediates proapoptotic signaling, thus may be used prevent injuries clinical settings.