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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.1
- 수록면
- 672 - 685 (14page)
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초록· 키워드
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Currently, liver transplantation is the only available remedy for patients with end-stage liver disease. Conservation of transplanted liver graft is the most important issue as it directly related to patient survival. Carbonyl reductase 1 (CBR1) protects cells against oxidative stress and cell death by inactivating cellular membrane-derived lipid aldehydes. Ischemia-reperfusion (I/R) injury during living-donor liver transplantation is known to form reactive oxygen species. Thus, the objective of this study was to investigate whether CBR1 transcription might be increased during liver I/R injury and whether such increase might protect liver against I/R injury. Our results revealed that transcription factor Nrf2 could induce CBR1 transcription in liver of mice during I/R. Pre-treatment with sulforaphane, an activator of Nrf2, increased CBR1 expression, decreased liver enzymes such as aspartate aminotransferase and alanine transaminase, and reduced I/R-related pathological changes. Using oxygen-glucose deprivation and recovery model of human normal liver cell line, it was found that oxidative stress markers and lipid peroxidation products were significantly lowered in cells overexpressing CBR1. Conversely, CBR1 knockdown cells expressed elevated levels of oxidative stress proteins compared to the parental cell line. We also observed that Nrf2 and CBR1 were overexpressed during liver transplantation in clinical samples. These results suggest that CBR1 expression during liver I/R injury is regulated by transcription factor Nrf2. In addition, CBR1 can reduce free radicals and prevent lipid peroxidation. Taken together, CBR1 induction might be a therapeutic strategy for relieving liver I/R injury during liver transplantation.
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참고문헌 (42)
참고문헌 신청
Amersi, F. / 1999 / Upregulation of heme oxygenase-1 protects genetically fat Zucker rat livers from ischemia/reperfusion injury / J. Clin. Invest 104:1631~1639
Chian, S. / 2014 / Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo / Biochem. Biophys. Res. Commun 447:602~608
Chowdhry, S. / 2010 / Loss of Nrf2markedly exacerbates nonalcoholic steatohepatitis / Free Radic. Biol. Med 48:357~371
Clavien, P. A. / 2001 / Mechanism of hepatocyte death after ischemia : apoptosis versus necrosis / Hepatology 33:1555~1556
Ellis, E. M. / 2007 / Reactive carbonyls and oxidative stress : potential for therapeutic intervention / Pharmacol. Ther 115:13~24
Chian, S. / 2014 / Luteolin inhibits the Nrf2 signaling pathway and tumor growth in vivo / Biochem. Biophys. Res. Commun 447:602~608
Chowdhry, S. / 2010 / Loss of Nrf2markedly exacerbates nonalcoholic steatohepatitis / Free Radic. Biol. Med 48:357~371
Clavien, P. A. / 2001 / Mechanism of hepatocyte death after ischemia : apoptosis versus necrosis / Hepatology 33:1555~1556
Ellis, E. M. / 2007 / Reactive carbonyls and oxidative stress : potential for therapeutic intervention / Pharmacol. Ther 115:13~24
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