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2015 ; 5
(ä): 14816
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The protein kinase 2 inhibitor tetrabromobenzotriazole protects against renal
ischemia reperfusion injury
#MMPMID26423352
Ka SO
; Hwang HP
; Jang JH
; Hyuk Bang I
; Bae UJ
; Yu HC
; Cho BH
; Park BH
Sci Rep
2015[Oct]; 5
(ä): 14816
PMID26423352
show ga
Protein kinase 2 (CK2) activation was reported to enhance reactive oxygen species
production and activate the nuclear factor ?B (NF-?B) pathway. Because oxidative
stress and inflammation are critical events for tissue destruction during
ischemia reperfusion (I/R), we sought to determine whether CK2 was important in
the renal response to I/R. Mice underwent 25 min of renal ischemia and were then
reperfused. We confirmed an increased expression of CK2? during the reperfusion
period, while expression of CK2? remained consistent. We administered
tetrabromobenzotriazole (TBBt), a selective CK2? inhibitor before inducing I/R
injury. Mice subjected to I/R injury showed typical patterns of acute kidney
injury; blood urea nitrogen and serum creatinine levels, tubular necrosis and
apoptosis, inflammatory cell infiltration and proinflammatory cytokine
production, and oxidative stress were markedly increased when compared to sham
mice. However, pretreatment with TBBt abolished these changes and improved renal
function and architecture. Similar renoprotective effects of CK2? inhibition were
observed for emodin. Renoprotective effects of CK2? inhibition were associated
with suppression of NF-?B and mitogen activated protein kinase (MAPK) pathways.
Taken together, these results suggest that CK2? mediates proapoptotic and
proinflammatory signaling, thus the CK2? inhibitor may be used to prevent renal
I/R injuries observed in clinical settings.