首页 / 资料库 / 文献详情

[Effect of Emodin Derivative E11 on T Lymphocytic Leukemia Cell Line Molt-4 and Its Possible Mechanisms].

Yuling HuangWenfeng WangJianda HuJun-Ting ZhengJing Li

2016PubMedAgricultural and Biological Sciences被引 1

出版方页面 →

摘要

OBJECTIVE: To explore the effect of a new emodin derivative E11 on proliferation and apoptosis of T lymphocytic leukemia cell line Molt-4 and its possible mechanisms. METHODS: MTT method was used to plot cell growth curve. Colony culture assay was performed for studying the effect of emodin derivative E11 on colony-formation of Molt-4. The fluorescent microscopy with DAPI staining was used to examine the cell morphological changes after E11 treatment. DNA fragmentation method was used to detect the inducing effect of emodin derivative E11 on cell apoptosis. Western blot was used to determine the expressions of apoptosis-related proteins including procaspase-9, procaspase-3, PARP and PI3K/AKT, MAPK signalling pathway. RESULTS: Emodin derivative E11 could strongly inhibit the growth of Molt-4 with the IC50 in 48 h at 1.381 ± 0.1552 µmol/L in dose-dependent manner. 0.1 µmol/L of E11 could inhibit cell colony formation. The typrical apopototic morphologic changes of Molt cells treated with E11 could be observed under fluorescence microscope with DAPI staining. DNA apoptotic ladder could be observed by DNA fragmentation.The expressions of procaspase -9, procaspase-3, PARP, p-MAPK, p-AKT, mTOR, p-mTOR, p-P70 and p-4BEP1 were down-regulated, while expressions of MAPK, AKT, 4EBP1 and P70 were not changed remarkably after Molt-4 were treated with E11 for 48 h. CONCLUSION: E11 can remarkably inhibit the proliferation and induce the apoptosis of Molt-4 cells. The mechanism of apoptosis of Molt-4 cells may be related with the suppression of PI3K/AKT and MAPK signalling pathways.

引用本文(GB/T 7714)

Yuling Huang, Wenfeng Wang, Jianda Hu, 等. [Effect of Emodin Derivative E11 on T Lymphocytic Leukemia Cell Line Molt-4 and Its Possible Mechanisms].[J]. PubMed, 2016.

引文网络

参考文献与被引分析加载中…

DOI:https://doi.org/10.7534/j.issn.1009-2137.2016.01.002

本站仅收录题录与摘要供学习参考,全文版权归属出版方;如有侵权请联系我们删除。