Effect of Ketamine on Apoptosis by Energy Deprivation in Astroglioma Cells using Flow Cytometry System
Apoptosis is a programmed, physiologic mode of cell death that plays an important role in tissue homeostasis. As for the central nervous system, ischemic insults can induce pathophysiologic cascade of apoptosis in neurophils. Impairment of astroc-tye functions during brain ischemia can critically in...
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Published in | Journal of Korean medical science p. 113 |
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Main Authors | , , , |
Format | Journal Article |
Language | Korean |
Published |
대한의학회
01.02.2005
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Subjects | |
Online Access | Get full text |
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Summary: | Apoptosis is a programmed, physiologic mode of cell death that plays an important
role in tissue homeostasis. As for the central nervous system, ischemic insults can
induce pathophysiologic cascade of apoptosis in neurophils. Impairment of astroc-tye functions during brain ischemia can critically influence neuron survival by neuron-glia interactions. We aimed to elucidate the protective effect of ketamine on apop-tosis by energy deprivation in astrocytes. Ischemic insults was induced with iodoac-etate/ carbonylcyanide m-chlorophenylhydrazone (IAA/CCCP) 1.5 mM/ 20 M or 150 M/2 M for 1 hr in the HTB-15 and CRL-1690 astrocytoma cells. Then these cells were reperfused with normal media or ketamine (0.1 mM) containing media for 1 hr or 24 hr. FITC-annexin-V staining and propidium iodide binding were determined by using flow cytometry. Cell size and granularity were measured by forward and side light scattering properties of flow cytometry system, respectively. An addition of keta-mine during reperfusion increased the proportion of viable cells. Ketamine alleviated cell shrinkage and increased granularity during the early period, and ameliorated cell swelling during the late reperfusion period. Ketamine may have a valuable effect on amelioration of early and late apoptosis in the astrocytoma cells, even though the exact mechanism remains to be verified. KCI Citation Count: 3 |
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Bibliography: | G704-000345.2005.20.1.019 http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0191120050200010113 |
ISSN: | 1011-8934 1598-6357 |