摘要
目的探讨P3 8α在蛋白酶体抑制剂3,4-二氯异香豆素(3,4-Dichloroisocoumarin,DCI)诱导人胃癌细胞BGC8 2 3凋亡过程中作用。方法采用MTT,流式细胞术、分析DCI对细胞凋亡的诱导作用,RT-PCR分析DCI作用于胃癌细胞后P3 8 MAPK在基因表达水平改变的情况。结果随着DIC浓度的增加和处理时间延长,胃癌细胞增殖明显受到抑制,4 0 0μmol.L?1DCI作用于胃癌细胞2 4 h后细胞存活率4 3.6±5.3%,与对照组比较差异显著(P(0.0 1)。流式细胞术显示DCI主要作用于S期细胞,3 0 0μmol.L?1DCI浓度时,细胞凋亡率2 3.8 6%,与对照组比较差异明显(P(0.0 5)。3 0 0、1 5 0μmol.L?1DCI作用于胃癌细胞后均可以使P3 8α基因灰度值明显高于对照组,差异有显著性(P(0.0 1)。结论DCI可抑制人胃癌BGC8 2 3细胞增殖并促进其凋亡,在此过程中P3 8α通路激活发挥重要作用。
Objective To explore relationship between the expression of P38a and apoptosis of cells BGC823 induced by DCI（3,4-Dichloroisocoumarin）. Methods MTT assay was used to calculate the cell inhibition rate ,AnnexinV / PI staining was used to determine the apoptosis rate. The expression of P38a was determined by RT-PCR. Results DCI inhibited BGC823 cell growth significantly with the raised concentration and prolonged treatment of DCL The survival rate of BGC- 823was 43.6±5.3% after treating by 400μmol · L^-1 DCI. There was significant differences comparing with control group. Flow cytometric analysis display that DCI have an effect on the S stage cell. The apoptosis rate of group DCI （300 μmol· L^-1 ）was significant,which was reached to 23.86% . There were significant differences between group DCI and control group （P 〈 0.01）. The expression of P38 gene is higher in group DCI （300μmol · L^- 1and 150μmol · L^-1 ） than that of the control group（P 〈 0.01）. Conclusions DCI can significantly inhibit prolification of BGC823 cells in vitro and induce them injury and apoptosis. High expression of P38a gene caused by DCI were related to cells＇ injury and apoptosis.
出处
《实用肿瘤学杂志》
CAS
2008年第4期322-325,共4页
Practical Oncology Journal
关键词
胃癌
蛋白酶体抑制剂
P38
Gastric neoplasms
Proteasome inhibitors
P38
