Aim To observe effects of breviscapine on lymphocyte proliferation and K562 cell death caused by doxorubicin.Methods The cell proliferation was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay,the p53/bcl-2 expression were assessed by western blotting,cell apoptosis was quantitated by Histone/DNA ELISA and flow cytometry,cytochrome C release was determined by ELISA,caspase-8 and caspase-3 activation were examined by colorimetric assay.Results Breviscapine could obviously enhance mouse lymphocyte proliferation and its resistance to doxorubicin,promote growth inhibition,cytochrome C release,caspase-8 and caspase-3 activation in K562 cells which were caused by doxorubicin,upregulate radio of p53/bcl-2 expression,and increase cell apoptosis.Conclusion Breviscapine was able to enhance antitumor effect of doxorubicin,the major mechanism by which breviscapine could promote sensitivity of tumor cell to chemotherapeutic agents might be related to activated apoptosis signal way.

Aim To study antiangiogenesis and antitumor of thalidomide.Methods In HUVECs, cell viability was determined by MTT assay;death type was observed by electron microscope; ratio of apoptosis was quantitated by flow cytometry.Angiogenesis was tested in chicken embryo chorioallantoic membrane.Effect of thalidomide on S_(180) was examined in homograft mice and microvascular counts were detected through immunochemical staining method.Results Thalidomide might inhibite the growth of HUVECs with a IC_(50) value of(22.91?1.74) ?mol?L~(-1),cells treated by thalidomide for 48 h displayed morphological characteristics of different stages associated with apoptosis,which were irregular nucleus, condensed chromatin, ballooning endoplasmic reticulum, apoptotic bodies,under electron microscope.Thalidomide might be able to cause apoptosis or necrosis of HUVECs in flow cytometry and raised positive of antiangiogenesis with increasing of dosage in chicken embryo chorioallantoic membrane. Thalidomide as a single agent might not significantly prevent tumor growth but decrease microvascular counts in tumors, however, in combination with cyclophosphamide, thalidomide could decrease dosage of cyclophosphamide and enhance antitumor of cyclophosphamide.Conclusion Thalidomide might hold back angiogenesis,as a single agent, could not significantly prevent S_(180) tumor from growing,but acted synergistically with cyclophosphamide.