Δ9‐Tetrahydrocannabinol induces apoptosis in C6 glioma cells

FEBS Letters

Guzmán, Manuel¹  Galve-Roperh, Ismael¹  Canova, Cecile²  Brachet, Philippe³  Sánchez, Cristina¹ 

[1] Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain;INSERM U298, Centre Hospitalier Universitaire, 49033 Angers Cedex 01, France;INSERM U437, Centre Hospitalier Universitaire, 44093 Nantes Cedex 01, France

关键词: Cannabinoid;    Apoptosis;    Sphingomyelin hydrolysis;    Glioma cell;    MTT;    3-4;    5-dimethylthiazol-2;    5-diphenyltetrazolium bromide thiazol blue;    THC;    Δ9-tetrahydrocannabinol;   

DOI  :  10.1016/S0014-5793(98)01085-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Δ⁹-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-acetylsphingosine, 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 were 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.

【 授权许可】

Unknown