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目的通过体外实验研究半胱氨酸蛋白酶B(Cathepsin B)与紫杉醇诱导胃癌BGC-823细胞凋亡的关系。方法将BGC-823细胞(密度为1×105/孔)分别暴露于紫杉醇溶液(终浓度为0～0.5μmol/L)及紫杉醇(终浓度为0.3μmol/L)+Cathepsin B特异性抑制剂[CA-074(Me),终浓度为1.0μmol/L]48 h,并观察紫杉醇单独染毒组和紫杉醇+CA-074(Me)联合染毒组暴露6～48 h的细胞凋亡率和Cathepsin B的表达水平。结果随着紫杉醇染毒浓度的升高和染毒时间的延长,紫杉醇组和紫杉醇+CA-074(Me)组BGC-823细胞凋亡率和Cathepsin B表达水平呈上升趋势。与相同浓度、相同染毒时间紫杉醇组比较,紫杉醇+CA-074(Me)组BGC-823细胞凋亡率和Cathepsin B表达水平均较低,差异有统计学意义(P<0.05)。结论 Cathepsin B在紫杉醇诱导的细胞凋亡中发挥着一定的促进作用。
Objective To investigate the relationship between Cathepsin B and paclitaxel-induced apoptosis in BGC-823 gastric cancer cells in vitro. Methods BGC-823 cells (density 1 × 105 / well) were exposed to paclitaxel solution (final concentration 0 ~ 0.5μmol / L) and paclitaxel (final concentration 0.3μmol / L) + Cathepsin B specific inhibitor [ (CA-074 (Me), final concentration of 1.0μmol / L] for 48 h. The apoptotic rate and Cathepsin concentration of 6-48 h after paclitaxel + CA-074 (Me) B expression level. Results The apoptotic rate and the expression of Cathepsin B in paclitaxel group and paclitaxel + CA-074 (Me) group increased with the increase of paclitaxel concentration and exposure time. Compared with paclitaxel group, the apoptotic rate and the expression of Cathepsin B in paclitaxel + CA-074 (Me) group were significantly lower than those in paclitaxel group at the same concentration and same time (P <0.05). Conclusion Cathepsin B plays a role in promoting paclitaxel-induced apoptosis.