Δ9-tetrahydrocannabinol induces apoptosis in C6 glioma cells

被引:222
|
作者
Sánchez, C
Galve-Roperh, I
Canova, C
Brachet, P
Guzmán, M
机构
[1] Univ Complutense, Sch Biol, Dept Biochem & Mol Biol 1, E-28040 Madrid, Spain
[2] CHU Angers, INSERM U298, F-49033 Angers 01, France
[3] CHU Nantes, INSERM U437, F-44093 Nantes 01, France
关键词
cannabinoid; apoptosis; sphingomyelin hydrolysis; glioma cell;
D O I
10.1016/S0014-5793(98)01085-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Delta(9)-Tetrahydrocannabinol (THC), the major active component of marijuana, induced apoptosis in C6.9 glioma cells, as determined by DNA fragmentation and loss of plasma membrane asymmetry. THC stimulated sphingomyelin hydrolysis in C6.9 glioma cells. THC and N-acetglsphingosine, a cell-permeable ceramide analog, induced apoptosis in several transformed neural cells but not in primary astrocytes or neurons. Although glioma C6.9 cells expressed the CB1 cannabinoid receptor, neither THC-induced apoptosis nor THC-induced sphingomyelin breakdown mere prevented by SR141716, a specific antagonist of that receptor. Results thus show that THC-induced apoptosis in glioma C6.9 cells may rely on a CB1 receptor-independent stimulation of sphingomyelin breakdown. (C) 1998 Federation of European Biochemical Societies.
引用
收藏
页码:6 / 10
页数:5
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