논문 해외 국제전문학술지(SCI급) PHLOROFUCOFUROECKOL IMPROVES GLUTAMATE-INDUCED NEUROTOXICITY THROUGH MODULATION OF OXIDATIVE STRESS-MEDIATED MITOCHONDRIAL DYSFUNCTION IN PC12 CELLS
- 학술지 구분 국제전문학술지(SCI급)
- 게재년월 2016-00
- 저자명 KIM, JJ (KIM, JWA-JIN),이봉호공동(참여),KIM, DK (KIM, DO-KYUNG),YOO, YC (YOO, YUNG CHOON),LEE, KB (LEE, KYUNG BOK),LEE, JW (LEE, JAE WON),BAK, DH (BAK, DONG-HO),SHIN, SA (SHIN, SUN-AE),KANG, YJ (KANG, YOON-JOONG),YUK, JM (YUK, JAE-MIN)...MORE,JO, EK (JO, EUN-KYEONG),LEE, J (LEE, JINA),KIM, DW (KIM, DONG WOON)
- 학술지명 PLOS ONE
- 발행처명 PUBLIC LIBRARY SCIENCE
- 발행국가 해외
- 논문언어 외국어
홈페이지논문 초록 (Abstract)
Stroke is a complex neurodegenerative disorder with a clinically high prevalence and mortality. Despite many efforts to protect against ischemic stroke, its incidence and related permanent disabilities continue to increase. In this study, we found that pretreatment with phlorofucofuroeckol (PFF), isolated from brown algae species, significantly increased cell viability in glutamate-stimulated PC12 cells. Additionally, glutamate-stimulated cells showed irregular morphology, but PFF pretreatment resulted in improved cell morphology, which resembled that in cells cultured under normal conditions. We further showed that PFF pretreatment effectively inhibited glutamate-induced apoptotic cell death in a caspase-dependent manner. Reactive oxygen species (ROS) induced by oxidative stress are closely associated with ischemia-induced neurological diseases. Exposure of PC12 cells to glutamate induced abundant production of intracellular ROS and mitochondrial dysfunction, which was attenuated by PFF in a dose-dependent manner. In vivo studies revealed that PFF-mediated prevention was achieved predominantly through inhibition of apoptosis and mitochondrial ROS generation. Taken together, these results suggest the possibility of PFF as a neuroprotective agent in ischemic stroke.