저산소 및 저포도당에 의한 혈관내피세포의 세포사멸에 대한 Ofloxacin의 억제효과 및 그 작용기전에 관한 연구
Ofloxacin Inhibits Hypoxia/Hypoglycemia-Induced Apoptosis in Bovine Aortic Endothelial Cells
김해선, 이유미, 유미애, 이종원, 류석환, 김규원,
소속 상세정보
김해선 ( Kim Hae-Sun )
부산대학교 분자생물학과
이유미 ( Lee You-Mie )
부산대학교 분자생물학과
유미애 ( Yoo Mi-Ae )
부산대학교 분자생물학과
이종원 ( Lee Jong-Won )
대구가톨릭대학교 의과대학 생화학교실
류석환 ( Ryu Seuk-Hwan )
대구가톨릭대학교 의과대학 정신과학교실
김규원 ( Kim Kyu-Won )
서울대학교 약학대학
KMID : 0603520010060030155
Abstract
Hypoxia/hypoglycemia can cause apoptosis, an important feature in the progression of ischemic diseases such as ischemic infarction, stroke and athroscleosis. It was reported that previous use of the flouquinolone type antibiotic ofloxacin decreases the risk of developing acute myocardial infarction. On the basis of previous reports, we hypothesize that ofloxacin may prolong survival of endothelial cells against hypoxia/hypoglycemia-induced apoptosis. The ofloxacin treatment increased the viability of BAECs (Bovine Aortic Endothelial Cells) exposured to hypoxia/hypoglycemia for 48h compared with the control. Ofloxacin reduced the DNA fragmentation and the nuclear condensation. By using FACSscan analysis after PI staining, we found that the proportion of apoptotic subdiploid cells was decreased by the treatment of ofloxacin under hypoxia/hypoglycemia. In order to investigate the anti-apoptotic mechanism of ofloxacin under hypoxia/hypoglycemia, we examined the expression levels of antiapoptotic protein Bc1-2 and proapoptotic protein Bax by immunoblot analysis. The treatment of ofloxacin induced the relatively higher expression levels of Bc1-2 in BAECs under hypoxia/hypoglycemia. However, the expression levels of Bax were not changed. Taken together, these results suggest that ofloxacin inhibits hypoxia/hypoglycemia-induced apoptosis and increases the viability of BAECs through enhancement of Bc1-2 protein expression under hypoxia/hypoglycemia.
키워드
Ofloxacin; Hypoxia; Hypoglycemia; Apoptosis
원문 및 링크아웃 정보
등재저널 정보