阿霉素诱导胰腺癌BxPC-3细胞凋亡过程中p38MAPK的表达

A study on p38MAPK expression in the course of the pancreatic cancer cell BxPC-3 apoptosis induced by adriamycin

目的研究阿霉素诱导胰腺癌细胞凋亡过程中p38MAPK表达的变化,探讨p38MAPK在其中的作用。方法用膜联蛋白V-PI(annexinV-PI)染色及流式细胞技术分析阿霉素及应用p38MAPK抑制剂SB203580对胰腺癌细胞凋亡的影响,同时利用免疫细胞化学法观察经阿霉素及SB203580处理人胰腺癌BxPC-3细胞后,p38MAPK的表达水平。结果SB203580(20μmol/L)干预组胰腺癌BxPC-3细胞凋亡率为(20.1±1.4)%,阿霉素作用24 h后诱导胰腺癌BxPC-3细胞凋亡,凋亡率为(31.1±2.7)%,加用SB203580抑制p38MAPK通路后可增强阿霉素诱导的凋亡作用,凋亡率达(40.4±2.6)%。采用单因素方差分析F=136.79,组间比较组与组之间差异有统计学意义。以20μmol/L阿霉素作用BxPC-3胰腺癌细胞24 h后可见p38MAPK在细胞染色后呈现深褐色颗粒散在分布于部分或整个细胞核及细胞质内,联合应用SB203580后可见p38MAPK表达颗粒密度减低,数量减少。结论阿霉素可以活化p38MAPK通路,p38MAPK可能起到保护胰腺癌BxPC-3细胞逃避阿霉素诱导的凋亡,阻断该通路可增强阿霉素诱导胰腺癌细胞凋亡的作用。

Objective To study the p38MAPK expression change in the course of pancreatic cancer cells apoptosis induced by adriamycin（ADM）. Methods The effect of ADM and SB203580 on the apoptosis was analysed with annexinV-PI staining and flow cytometry, detecting the effect of ADM and SB203580 on the p38MAPK expression with cytoimmunochemistry. Results ①After ADM 24 h＇s action the BxPC-3＇s apoptosis rate was 20.1%, higher than the control group （P〈0.01）; the group of ADM combining SB203580 got a cell apoptosis rate 40.9%, higher markedly than the groups with single ADM did; SB203580 increased the ADM＇s apoptosis-indueing activity; the F value was 136.79 according to the one way analysis of variance（ANOVA）. ② p38MAPK was located in the cell plasma, showing deep brown, when adding 20 μmol/L ADM to BxPC-3 cell for 24 h; the p38MAPK expression decreased; density and count of the p38MAPK all declined after adding 20μmol/L ADM and SB203580. Conclusion ADM can activate the p38MAPK signal way, p38MAPK can protect BxPC-3 from the apoptosis induced by ADM, blocking the p38MAPK signal way can increase the apoptosis induced by ADM.