Effects of aminophylline on proliferation and apoptosis in Raji lympho-blastoid cell line.
- Author:
Ze-Lin LIU
1
;
Zuo-Ren DONG
;
Xue-Jun ZHANG
;
Fu-Xu WANG
;
Jing-Ci YANG
;
Wei-Dong MA
;
Xing-Yan DU
;
Li YAO
Author Information
1. Department of Hematology, The Second Hospital, Hebei Medical University, Shijiazhuang 050000, China.
- Publication Type:Journal Article
- MeSH:
Aminophylline;
pharmacology;
Apoptosis;
drug effects;
Burkitt Lymphoma;
drug therapy;
genetics;
pathology;
Cell Division;
drug effects;
Cyclin B;
genetics;
metabolism;
Cyclin B1;
Dose-Response Relationship, Drug;
Flow Cytometry;
Gene Expression Regulation, Neoplastic;
drug effects;
Humans;
Intracellular Membranes;
drug effects;
physiology;
Membrane Potentials;
drug effects;
Mitochondria;
drug effects;
physiology;
Phosphodiesterase Inhibitors;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
genetics;
metabolism;
RNA, Messenger;
drug effects;
genetics;
metabolism;
S Phase;
Tumor Cells, Cultured;
drug effects;
metabolism;
ultrastructure
- From:
Journal of Experimental Hematology
2003;11(1):45-49
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate whether and how phosphodiesterase (PDE) inhibitors modulate the proliferation, cell cycle and apoptosis in lymphoma cells. The effects of aminophylline (AM), a non-specific PDE inhibitor, on Raji cells were explored in vitro. MTT assay, light and transmission electron microscopy and annexin V staining were used to observe cell proliferation, morphologic changes and apoptosis rate in AM-treated cells, and FCM and RT-PCR techniques were adopted to detect the effect on cell cycle, the expression of cyclin B1 and Bcl-2 and mitochondrial transmembrane potential in AM-treated cells. The results showed that AM inhibited the growth of Raji cells in a concentration-dependent manner. Morphologic observations showed apoptosis changes in AM-treated cells, including cytoplamic shrinkage, cytoplasmic bubbling, karyopyknosis and nuclear fragmentation. FCM and RT-PCR detection showed that AM intervention increased the fraction of annexin V(+) cells, reduced the value of mitochondrial transmembrane potential, induced S phase arrest, and down-regulated the expression of Bcl-2 at both mRNA and protein level and cyclin B1 protein in a concentration-dependent manner. It is concluded that PDE inhibitor aminophylline may induce Raji cell growth inhibition, S phase arrest, apoptosis via down-regulation of Bcl-2 and reduction of mitochondrial transmembrane potential.
