RÉSUMÉ
<p><b>OBJECTIVE</b>Efficacy of HSV-tk/GCV system antitumor effects was assessed on human laryngeal cancer cell line Hep-2 in vitro. To assess the HSV-tk/CGV system whether has an antitumour effect on human laryngeal squamous cell cancer Hep-2 in vitro. The mechanisms of cytotoxity were also assessed.</p><p><b>METHODS</b>Hep-2 cells were transfected with HSV-tk gene by lipofection. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the HSV-tk gene expression. MTT was utilized to test for the cytotoxicity of this system. The cell-circle arrest and apoptosis were analyzed by flowcytometry assay.</p><p><b>RESULTS</b>HSV-tk gene transfected cells demonstrated obvious cytoreductivity followed by ganciclovir (GCV) administration and this cytoreductivity showed partial GCV dose-independent. HSV-tk gene transfected cells demonstrated obvious s-phase arrest, no apoptosis and necrosis occurred.</p><p><b>CONCLUSIONS</b>The HSV-tk/GCV system can inhabit the growth of Hep-2 cells effectively. S-phase arrest perhaps is the main reason that leads to the cell inhibition in our study. HSV-tk/GCV system has potential antitumor effects for the future clinical practice.</p>
Sujet(s)
Humains , Carcinome épidermoïde , Thérapeutique , Lignée cellulaire tumorale , Ganciclovir , Gènes-suicide transgéniques , Thérapie génétique , Vecteurs génétiques , Tumeurs du larynx , Thérapeutique , Simplexvirus , Génétique , Thymidine kinase , Génétique , TransfectionRÉSUMÉ
<p><b>OBJECTIVE</b>To study the effect of icariin on vascular endothelial cells (VECs) injury induced by hypoxia.</p><p><b>METHODS</b>The hypoxia-ischemia model was established. The effect of icariin on injury of VECs activity induced by hypoxia was determined by MTT assay. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) activity in cell homogenate were measured with corresponding kit. Effect of icariin on cells apoptosis induced by hypoxia was determined by Hoechst 33342 fluorescent staining, cell ultrastructure observation under transmission electron microscopy and analysis on gene fragmentation by flow cytometry and DNA gel electrophoresis.</p><p><b>RESULTS</b>ICA could inhibit the hypoxia induced VECs reduction, suppress LDH activity, reduce the MDA production, and enhance SOD activity under hypoxia. Hypoxia could induce VECs apoptosis, revealed chromation condensed in nuclei with the fragments arranged along the nuclear membrane. DNA gel electrophoresis showed typical ladder strands of DNA. Cells displayed a typical sub-diploid peak in flow cytometry. ICA could significantly inhibit the hypoxia induced apoptosis of VECs.</p><p><b>CONCLUSION</b>ICA has the protective effect on hypoxia injured VECs, which may be related to its effect of anti-apoptosis, anti-lipid peroxidation and SOD activity enhancing.</p>