Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add filters








Language
Year range
1.
Chinese Journal of Oncology ; (12): 216-219, 2003.
Article in Chinese | WPRIM | ID: wpr-347458

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the relation between activation of NF-kappa B and chemotherapy induced apoptosis of leukemic cells and the effect of vincristine (VCR) on them.</p><p><b>METHODS</b>Electrophoretic mobility shift assay (EMSA) was used to detect the activation of NF-kappa B and tunel DNA electrophoresis was adopted to observe the apoptosis induced by cytosine arabinoside (Ara-C) and etopside (Vp-16) in P388 leukemic cells.</p><p><b>RESULTS</b>The activation of NF-kappa B induced by Ara-C and Vp-16 was obviously correlated to apoptosis in P388 cells. VCR (0.1 micromol/L) could suppress activation of NF-kappa B by 52% and 63% and significantly increase the apoptosis by 89% and 123% as induced by Ara-C (100 micromol/L) and Vp-16 (100 micromol/L). The activity of NF-kappa B could be found in P388 cells before being exposed to chemotherapeutic agent.</p><p><b>CONCLUSION</b>Chemotherapeutic agents can induce apoptosis and activation of NF-kappa B of P388 cells. The mechanism of VCR potentiating chemotherapeutics induction of leukemia cell apoptosis may be related to its suppression of the NF-kappa B activity in the P388 cells.</p>


Subject(s)
Animals , Mice , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , In Situ Nick-End Labeling , Leukemia P388 , Drug Therapy , Pathology , NF-kappa B , Metabolism , Vincristine , Pharmacology
SELECTION OF CITATIONS
SEARCH DETAIL