Protective Effect of PKC and Nitric Oxide Affecting Taxol-Induced Cytotoxicity in C6-Gial Cells.
- Author:
Heung Jae LEE
1
;
Sang Chul KWAN
;
Han Sol LEE
;
Jung Mu HUR
;
Deok Hwa CHOI
;
Jay Min OH
;
Jeong Joong KIM
;
Min Kyu CHOI
;
Yeun Tai CHUNG
Author Information
1. Department of Anatomy, Wonkwang University School of Medicine, Iksan, Korea. mkchoi@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Taxol;
C6-glial cell;
Protein kinase C;
Nitrc oxide
- MeSH:
Apoptosis;
Caspase 3;
Cell Cycle;
Cell Death;
Hand;
Humans;
Myristic Acid;
Nitric Oxide*;
Nitroprusside;
Paclitaxel;
Protein Kinase C;
Signal Transduction
- From:Korean Journal of Anatomy
2003;36(5):363-370
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Paclitaxel (Taxol) is known as effective drug for inhibition of cell cycle encouraging in human cancer cells. This drug named an antimicrotubule agent which simulate the mitotic arrest towards an apoptosis. The influence of phorbol 12 myristate 13 acetate (PMA) activated protein kinase C (PKC) and nitric oxide (NO) on taxol-induced apoptosis, is poorly understood. To investigate the effects of PMA and NO on the signal transduction in taxol-induced apoptosis in C6-glial cells, the viability and caspase-3 activity of C6-glial cells were analyzed. Pretreatement with PKC activatior (PMA) protected taxol-induced cell death in C6-glial cells, by inhibited caspases-3 activity. On the other hand, the taxol-induced apoptosis was highly enhanced by sodium nitroprusside (SNP) and lipopolysaccharide (LPS), as NO activator. These results suggest that PMA strongly blocks the apoptotic effect of taxol, while nitric oxide has no protective effects in the process of toxol-induced apoptosis in C6-glial cells.
