Effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expression of SHIP mRNA / 中国实验血液学杂志

This study was aimed to investigate the effects of bortezomib combined with 5-azacytidine on the apoptosis of K562 cells and expressiom of SHIP mRNA. The K562 cells were cultured and treated with different concentrations of bortezomib, 5-azacytidine or their combination for 24 hours. Then, the expression of SHIP mRNA was detected by RT-PCR,the cell proliferation was analyzed by using MTT assay and flow cytometry. The results showed that 5-20 nmol/L bortezomib could effectively inhibit the proliferation of K562 and this inhibitory effect gradually enhanced along with the increase of bortezomib concentration, the group of bortezomib combined with 5-azacytidine showed more inhibitory effect on K562 cells than that of bortezomib or 5-azacytidine alone.The bortezomib could promote the apoptosis of K562 cells in a dose-dependent manner,and this apoptotic effect was higher in group of bortezomib combined with 5-azacytidine than that in group of bortezomib or 5-azacytidine alone.Bortezomib could down-regulated the expression of SHIP mRNA in a dose-dependent manner,and this down-requlated effect was higher in group of bortezomib combined with 5-azacytidine than that in group of bortezomib or 5-azacytidine alone.It is concluded that bortezomib and 5-azacytidine can induce apoptosis by inhibiting the expression of SHIP mRNA in K562 cells.The combination of bortezomib with 5-azacytidine displays a synergetic effect.

Effect of proteasome inhibitor bortezomib on proliferation, apoptosis and SHIP gene expression in K562 cells / 中国实验血液学杂志

This study was aimed to investigate the effects of proteasome inhibitor bortezomib on proliferation, apoptosis and the SHIP expression of K562 cells. K562 cells were treated with bortezomib of different concentrations. Cell proliferation was analyzed by MTT assay, cell apoptosis was detected by flow cytometry and SHIP mRNA expression was assayed by RT-PCR.The results showed that after being treated with 10, 20, 50 and 100 nmol/L bortezomib for 24 h, the inhibitory rates of K562 cells were (5.76 ± 1.47)%, (10.55 ± 1.59)%, (17.14 ± 2.05)% and (27.69 ± 3.57)% respectively, and were higher than that in control (1.30 ± 0.10); when K562 cells were treated with 20 nmol/L bortezomib for 24, 48 and 72 h, the inhibitory rates of cell proliferation were (10.55 ± 1.59)%, (16.33 ± 2.53)% and (19.78 ± 1.56)% respectively, there was statistic difference of cell proliferation rate between 24 h group and 48 h group (P < 0.05). After being treated with 10,20,50,100 nmol/L bortezomib for 24 h, the apoptotic rates of K562 cells were (12.7 ± 0.6)%, (26.9 ± 0.9)%, (32.6 ± 1.2)% and (72.5 ± 1.5)% respectively,and all higher than that in control (1.0 ± 0.5)% (P < 0.05). According to results of RT-PCR detection, the expression level of SHIP mRNA was obviously up-regulated after treatment with bortezomib, and showed statistical difference in comparison with control. It is concluded that bortezomib inhibits proliferation of K562 cells in time and concentration-dependent manner and induces apoptosis through up-regulation of SHIP gene.

Effect of T-2 toxin on apoptosis of fetus chondrocytes / 中国地方病学杂志

Objective　To investigate the effect of T-2 toxin on apoptosis of chondrocytes.Methods　Chondrocytes which were obtained from aborted fetal were cultured in vitro.Four days later,these chondrocytes were exposed to T-2 toxin in different concetrations for 16 hours.According to the concentratio ns,five experimental groups were divided:0,5,10,20,40 μg/L.Then TUNEL staining and Flowcytometry were used to detect the apoptosis of chondrocytes qualitativel y and quantitatively,the effect of T-2 toxin on proliferation of chondrocytes were also observed.Results　After being exposed to T-2 toxin,the body of chondrocytes shrinked obviously and there was a dose-dependent relationship bet ween the toxin concentration and the degree of shrink.The concentration of T-2 toxin changed from 0 μg/L to 10 ng/ml,the number of apoptosis increased.Conclusions　 T-2 toxin can inhibit the proliferation of chondroyte significantly in a dose-depenent manner. T-2 toxin can induce the apoptosis of chondrocyte and the numbers of apoptosis is proportionate to the concentration of T-2 toxin in particular range.