글로버메뉴 바로가기 본문 바로가기 하단메뉴 바로가기

논문검색은 역시 페이퍼서치

> 대한내과학회 > 대한내과학회 추계학술발표논문집 > 2014권 1호

Slide Session : OS-117 ; COPD : Neutrophil Elastase Suppresses Cigarette Smoke Extract-Induced Activation of Anti-Oxidative Pathway by Nrf2 Down-Regulation in Normal Human Bronchial Epithelial Cells

Slide Session : OS-117 ; COPD : Neutrophil Elastase Suppresses Cigarette Smoke Extract-Induced Activation of Anti-Oxidative Pathway by Nrf2 Down-Regulation in Normal Human Bronchial Epithelial Cells

( Tae Yun Park ) , ( Kyoung Hee Lee ) , ( Jiyeong Jeong ) , ( Chang Hoon Lee ) , ( Chul Gyu Yoo )

- 발행기관 : 대한내과학회

- 발행년도 : 2014

- 간행물 : 대한내과학회 추계학술발표논문집, 2014권 1호

- 페이지 : pp.441-441 ( 총 1 페이지 )


학술발표대회집, 워크숍 자료집 중 1,2 페이지 논문은 ‘요약’만 제공되는 경우가 있으니,

구매 전에 간행물명, 페이지 수 확인 부탁 드립니다.

1,000
논문제목
초록(외국어)
Background: Cigarette smoke (CS) induces lung infiammation and simultaneously activates anti-oxidative pathway as a defense mechanism. Recently, we found that neutrophil elastase (NE) enhances cigarette smoke extract (CSE)-induced infiammation. Therefore, this study was undertaken to investigate the roles of NE on CSE-induced activation of anti-oxidative pathway and its regulatory mechanism in normal human bronchial epithelial cells. Methods: BEAS-2B cells were used. Nrf2 activity assay using nuclear extracts was performed. The expression of heme oxygenase-1 (HO-1) or nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA was determined by real-time PCR. HO-1, Nrf2, DJ-1, or KEAP1 protein expressions were analyzed by Western blotting. Results: CSE activated Nrf2, a transcription factor, which regulates the expression of several antioxidants. CSE increased anti-oxidant, HO-1. Interestingly, NE suppressed CSE-induced expression of HO-1 mRNA and protein. Therefore, we first evaluated the effect of NE on Nrf2. Although NE did not affect the basal and inducible level of Nrf2 mRNA, it significantly decreased the expression of Nrf2 protein. Nrf2 protein stability has been reported to be regulated by DJ-1 and KEAP1. However, the expression level of DJ-1 and KEAP1 did not change in NE-treated cells. Nrf2 down-regulation by NE was not blocked by pre-treatment with proteasomal & lysosomal inhibitors (MG132, PS-341 & chloroquine, NH4Cl), pan-caspase inhibitor (zVAD-fmk), or ROS blocker (NAC). Conclusions: Taken together, these data suggest that NE accelerates CSE-induced damage in lung epithelial cells by blocking anti-oxidative pathway via down-regulation of Nrf2 at the post-translational step.

논문정보
  • - 주제 : 의약학분야 > 내과학
  • - 발행기관 : 대한내과학회
  • - 간행물 : 대한내과학회 추계학술발표논문집, 2014권 1호
  • - 발행년도 : 2014
  • - 페이지 : pp.441-441 ( 총 1 페이지 )
  • - UCI(KEPA) : I410-ECN-0102-2015-500-000133577
저널정보
  • - 주제 : 의약학분야 > 내과학
  • - 성격 : 학술발표
  • - 간기 : 연간
  • - 국내 등재 : -
  • - 해외 등재 : -
  • - ISSN :
  • - 수록범위 : 1998–2021
  • - 수록 논문수 : 17865