ABSTRACT
Cardiac dysfunction is a common and severe side-effect after cancer therapy including thoracic radiation or cytotoxic agents. With the development of the cancer therapy method and the agents, the survival time of the patients has improved while most cancer patients could live with tumor or even be cured. The rate of cancer therapeutics-related cardiac dysfunction have obviously increased which seriously affect the time and life quality of patients with tumor. But there are no authoritative consensus criteria or guideline to diagnose CTRCD at present while it is difficult to identify CTRCD with primary heart disease. In this article，we summarized some diagnosis methods which could identify early CTRCD，and then we may give early drug intervention as soon as possible to reduce the incidence and remission rate of cardiovascular events.
ABSTRACT
The aim of this study was to investigate the inhibitive effect of artesunate (ART) on CML cell line K562 and its influence on VEGF expression in vitro. Human CML cell line K562 cells were cultured in RPMI 1640 medium supplemented with 10% heat-inactivated fetal calf serum. All cells were cultured in a humidified atmosphere of 5% CO2 at 37.0 degrees C. K562 cells in logarithmic growth phase were collected and seeded in RPMI-1640 medium, and were treated with ART. At the indicated time points, viable cells were counted by trypan blue exclusion method. Each assay was triplicated. K562 cells were treated with ART at different concentrations. Morphological changes were observed with invert microscope. VEGF expression in K562 cells treated with ART at different concentrations and in the control group were detected by enzyme-linked immunosorbent assay (ELISA). The results indicated that ART obviously induced growth inhibition in K562 cells. The relationship between cell inhibition rates and the concentrations of ART showed a dose-dependent manner (p < 0.01). VEGF expression of K562 cells treated with ART at different concentrations decreased significantly (p < 0.01). No significant change of VEGF expression in control group was observed (p > 0.05), while VEGF expression was down-regulated significantly in experiment groups (p < 0.01). The inhibition rate of K562 cells increased in time and concentration-dependent manners. In K562 cell lines treated with ART, VEGF expression was up-regulated at first and then down-regulated to a lower level. It is concluded that ART inhibits k562 cell proliferation in a dose and time dependent manner. The mechanism underlying the inhibitive effect of ART on K562 cells may be realized through down-regulation of VEGF expression.