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논문분류	춘계학술대회 초록집
제목	Role of APE1/Ref-1 in hydrogen peroxide-induced apoptosis in human renal HK-2 cells
저자	Ha Yeon Kim* 1, Jung Sun Park2, Eun Hui Bae1, Seong Kwon Ma1, Jongun Lee2, Soo Wan Kim1
출판정보	2016; 2016(1):
키워드	APE1/Ref-1, APE1/Ref-1 inhibitor, Apoptosis, HK-2 cell, Ischemia-reperfusion injury
초록	Background: Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is multipotent protein that plays an essential role in the cellular response to oxdiative stress. In the present study, we investigated the role of APE1/Ref-1 in ischemia-refusion (IR) injury in rat kidney and hydrogen peroxide (H2O2) induced renal tubular apotosis. Methods: Kidney IR injury in rats was established by clamping the both renal arterys for 50 minutes followed by 2 or 5 days of reperfusion. Results: APE1/Ref-1 is predominantly localized in the nucleus in the kidney tubule cell, while there was lack of APE1/Ref-1 in the glomerulus. The fluorescence of APE1/Ref-1was most prominent in the proximal tubule. Consistenct with the expression of APE1/Ref-1, the level of APE1/Ref-1 protein also was highest in the cortex, modest in the outer meulla, and lowest in the inner medulla. In rat model of renal IR injury, the level of APE1/Ref-1 protein was increased compared with that in kidneys subjected to sham operation. We found that over-expression of APE1/Ref-1 in HK-2 cell enhanced the ratio of Bax/Bcl-2. The suppression of APE1/Ref-1 by the pharmacologic inhibitors E3330 in HK-2 cell with H2O2 exposure, resulted in decreased ratio of Bax/Bcl-2 and altered phosphorylation of ERK1/2, p38, JNK1/2, and NF-κB. Conclusion: These findings suggest that APE1/Ref-1 inhibitor attenuates H2O2-induced apoptosis in HK-2 cells by modulating the ERK/p38 signaling pathways.
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