유해활성산소 및 유해산화질소가 유발하는 핵과 소포체의 변화 분석

• 영문명: Analysis for Nucleus and Endoplasmic Reticulum Changes by Reactive Oxygen Species and Nitric Oxide
• 발행기관: 한국산업기술융합학회(구. 산업기술교육훈련학회)
• 저자명: 김연향(Yeon Hyang Kim) 정은영(Eun Young Jung) 정지윤(Ji Yun Jung) 정성오(Sung Oh Chung)
• 간행물 정보: 『산업기술연구논문지』산업기술교육훈련논문지 제19권 3호, 173~178쪽, 전체 6쪽
• 주제분류: 공학 > 공학일반
• 파일형태: PDF
• 발행일자: 2014.09.30

영문 초록

To investigate cross-talk between endoplasmic reticulum(ER) stress and oxidative stress in astroglioma, the cells were treated with hydrogen peroxide, DETA-NONOate and thapsigargin to raise intracellular levels of oxidative stress and ER stress, respectively. Cell viability was decreased in a dose-dependent manner in hydrogen peroxide- and DETA-NONOate - treated cells. Hydrogen peroxide, DETA-NONOate and thapsigargin also induced DNA fragmentation in these cells as indicated by terminal deoxynucleotidyl transferase-med iated dUTP nick end labeling. Hydrogen peroxide, DETA-NONOate and thapsigargin induced intracellular Ca2+ increase and perturbed Ca2+ homeostasis in endoplasmic reticulum(ER). Likewise, hydrogen peroxide, DETA-NONOate and thapsigargin also increased the expressions of ER stress- related molecules, IREl-a. The increase of IRE1 -a expression is coincided with those of p-JNK up on the treatment with hydrogen peroxide, DETA-NONOate, and thapsigargin in cells. These finding indicate that the increase of expression of IREl-a activating JNK pathway is induced during hydrogen peroxide, DETA-NONOate and thapsigargin - mediated cell death. Therefore, we conclude that oxidative stress including reactive oxygen species and nitric oxide cause nucleus and endoplasmic reticulum(ER) dysfunction and ER-related signals to occur in human astroglioma cells.

목차

I. 서 론

II. 실험재료 및 방법

III. 실험결과 및 고찰

IV. 결 론

참고문헌

키워드

Reactive Oxygen Species(유해활성산소) Nitric Oxide(유해산화질소) Astroglioma Cells(신경세포) Cell Death(세포사멸) Immune Regulation(면역조절)