ABSTRACT
OBJECTIVE@#To investigate the effect of Carfilzomib on mantle cell lymphoma (MCL), and to compare with effect of Bortezomib.@*METHODS@#The Jeko-1 cells and primary MCL cells were treated with Carfilzomib for 24, 48 and 72 h, then the inhibitory rate was detected using CCK-8. Lymphocytes derived from healthy volunteer were served as cell controls. Bortezomib and Cyclophosphamide (CTX) were served as medicinal controls. At the same time, the apoptosis of cells treated with different drugs was detected using flow cytometry.@*RESULTS@#The inhibitory effect of Carfilzomib on Jeko-1 cells and primary MCL cells was exhibited with time-dependent and concentration-dependent manners (P＜0.01, r=0.393, r=0.650, rJ=0.473, r=0.417), but the effect on lymphocytes derived from healthy volunteer only showed time-dependence (P＜0.01, r=0.928). Under the same concentration, Carfilzomib exhibited the proliferation Jeko-1 cells stronger than Bortezomib (P＜0.01), but the same inhibition on primary MCL cells was not significantly different from that on lymphocytes derived from healthy volunteer (P＞0.05). Under clinical recommended concentration, Carfilzomib had a stronger inhibitory effect on primary MCL cells than that of Bortezomib (P＜0.01). Cell apoptosis assay showed that under the same concentration the ability of Carfilzomib to induce cell apoptosis was significantly stronger than that of Bortezomib (P＜0.05).@*CONCLUSION@#Carfilzomib can inhibit the growth of MCL cells, its inhibitory rate on the MCL cells is higher than that of Bortezomib.
Subject(s)
Humans , Antineoplastic Agents , Apoptosis , Bortezomib , Cell Line, Tumor , Cell Proliferation , Lymphoma, Mantle-Cell , OligopeptidesABSTRACT
Objective In order to further optimize the cultivation program of clinical medicine undergraduates and promote the cultivation of medical students to adapt to the newest development. To understand and evaluate the post competency of clinical medical undergraduates and then establish a scientific and reasonable evaluation index system to further improve the quality of medical undergraduate talent training.Methods Combing with the Methods of literature research, Delphi method and hierarchical analysis, an evaluation index system of post competency of clinical undergraduate graduates based on the standard of clinical medicine professional certification is constructed .Results The evaluation index system of post competency of clinical graduates includes 4 first level indicators, 11 second level indicators and 63 third level indicators. The 4 first level can be divided into clinical ability, professional quality, science and scholarship., health and society by weight.Conclusion It is an effective way to cultivate medical talents to construct the evaluation index system of post competency of clinical undergraduates, which will contribute to the construction of "Healthy China".
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the neuroprotective effects of edaravone (Eda) on cobalt chloride (CoCl2)-induced oxidative stress and apoptosis in cultured PC12 cells as well as the underlying mechanisms.</p><p><b>METHODS</b>PC12 cells impaired by CoCl2 were used as the cell model of hypoxia. MTT (methyl thiazolyl tetrazolium) was used to assay the viability of the PC12 cells exposed to Eda with gradient concentrations; Hochest 33258 stain assay was used to analyze the apoptosis ratio of the PC12 cells; Bcl-2 and Bax protein levels in PC12 cells were examined by western blotting. ROS level, the mitochondrial transmembrane potential and caspase-3 activity in each group were detected by spectrofluorometer.</p><p><b>RESULTS</b>CoCl2 treatment caused the loss of cell viability in PC12 cells, which was associated with the elevation of apoptotic rate, the formation of ROS and the disruption of mitochondrial transmembrane potential. CoCl2 also significantly induced the upregulation of Bax/Bcl-2 ratio and the activation of caspase-3. In contrast, Eda significantly reversed these phenotypes, with its maximum protective effect at 0.1 micromol/L.</p><p><b>CONCLUSION</b>These results indicated that Eda could protect PC12 cells from CoCl2-induced cytotoxicity, and this protection might be ascribed to its anti-oxidative and anti-apoptotic activities.</p>