J Korean Neurol Assoc > Volume 13(1); 1995 > Article
Journal of the Korean Neurological Association 1995;13(1): 1-10.
칼슘길항제가 배양 백서 부신수질 갈색세포종 세포의 저산소 허혈에 미치는 영향
김병채, 신기춘, 손준호, 김요식, 조기현, 배원엽, 이기영, 김세종
전남대학교 신경과. 생화학교실
Effects of Calcium Antagonists on the PC12 Cell Damage Induced by Hypoxia
Byeong Chae Kim, M.D., Ki Chun Shin, M.D., Jun Ho Son, M.D., Yo Sik Kim, M.D., Ki Hyun Cho, M.D., Won Yeup Bae, M.D., Kee Young Lee, and Sei Jong Kim, M.D.
Department of Neurology and Biochemistry, Chonnam University Medical School
Abstract
Hypoxia-induced cell damage is known to be mediated by increase in intracellular calcium. In the present study, the effect of calcium channel blockers on the hypoxia-induced cell damage was investigated in iat pheochromocytoma cells line, PC12 cells. The cultured cells were exposed to hypoxia under 95% N2 plus 5% C02 gas phase and incubated in the media devoid of fetal bovine seruril The cell demage was assessed by measuring the release of lactate dehydrogenase (LDH) from the cells into the incubation media. Exposure of the cells to hypoxia for 2 hours caused a 28% of the total LDH to be released from cells -into media. The pretreatment of the cells with 1 mM each of diltiazem, nifedipine, and verapamil depressed the LDH release to the extent of 52%, 42%, and 30% inhibition, respectively. The inhibitory effects of diltiazem and verapamil were more marked at 1 mM than at 10 mM. The influx of 45 Ca2+ into the cells was rapidly increased within 2 minutes after exposure of the cells to hypoxia. Diltiazem at 1 mM almost completely inhibited Ca2+ influx, while nifedipine and verapamil exhibited only, 30% inhibition of Ca2- influx. The results lend support to the notion that mcreased intracellular calcium triggers a series of cascade reactions leadmg to cell death. It is suggested that the inhibitory effects of various calcium antagonists on hypoxia-induced cell damage differ from each other in their potency
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