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桔梗皂苷D对人胶质瘤U251细胞增殖、凋亡及PI3K/Akt信号通路的影响

Effects of platycodin D on proliferation, apoptosis and PI3K/Akt signal pathway of human glioma U251 cells.

作者信息

Xu Chong, Sun Guibo, Yuan Guangxin, Wang Rui, Sun Xiaobo

机构信息

Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Ministry of Education, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China.

Pharmaceutical College, Beihua University, Jilin 132013, China.

出版信息

Molecules. 2014 Dec 19;19(12):21411-23. doi: 10.3390/molecules191221411.

DOI:10.3390/molecules191221411
PMID:25532840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6270900/
Abstract

Effects of platycodin D (PD) on the proliferation, apoptosis and PI3K/Akt signaling pathway of human glioma U251 cells were investigated. Glioma U251 cells were treated with PD at final concentrations of 0, 16.3, 40.8, 81.6, 163.2 μM, and inhibition rate, early and late apoptotic rate, apoptotic index, expression of apoptosis-related proteins and phosphorylation of the PI3K/Akt signaling pathway were evaluated. The results showed that compared with the control group, PD could increase the proliferation inhibition rate of U251 cells in a dose- and time -dependent manner; PD could also elevate the early and late apoptotic rate, apoptotic index and the level of pro-apoptotic proteins of glioma U251 cells, such as Bax and cleaved caspase-3, but lower the level of apoptosis inhibitory protein, such as Bcl-2; PD could increase the ratio of G0/G1 phase U251 cells, and lower the proportion of Sphase U251 cells and the ratio of G2/M phase U251 cells; PD could reduce the ratio of p-Akt/Akt. The results indicate that PD can inhibit the proliferation, induce the apoptosis and cause the cell cycle arrest in human glioma U251 cells, which may be related to the inhibition of PD on the activation of PI3K/Akt signaling pathway.

摘要

研究了桔梗皂苷D（PD）对人胶质瘤U251细胞增殖、凋亡及PI3K/Akt信号通路的影响。用终浓度为0、16.3、40.8、81.6、163.2μM的PD处理胶质瘤U251细胞，并评估其抑制率、早期和晚期凋亡率、凋亡指数、凋亡相关蛋白表达以及PI3K/Akt信号通路的磷酸化情况。结果显示，与对照组相比，PD能以剂量和时间依赖性方式提高U251细胞的增殖抑制率；PD还能提高胶质瘤U251细胞的早期和晚期凋亡率、凋亡指数以及促凋亡蛋白水平，如Bax和裂解的caspase-3，但降低凋亡抑制蛋白水平，如Bcl-2；PD能增加G0/G1期U251细胞的比例，降低S期U251细胞的比例以及G2/M期U251细胞的比例；PD能降低p-Akt/Akt的比例。结果表明，PD可抑制人胶质瘤U251细胞的增殖，诱导其凋亡并导致细胞周期停滞，这可能与PD抑制PI3K/Akt信号通路的激活有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/1e17bc36480c/molecules-19-21411-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/f5e5e2384f47/molecules-19-21411-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/c6ccbf45be87/molecules-19-21411-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/6504f485e6c4/molecules-19-21411-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/87b06036f18a/molecules-19-21411-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/660b985e8e93/molecules-19-21411-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/0185dbc1247f/molecules-19-21411-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/1e17bc36480c/molecules-19-21411-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/f5e5e2384f47/molecules-19-21411-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/c6ccbf45be87/molecules-19-21411-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/6504f485e6c4/molecules-19-21411-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/87b06036f18a/molecules-19-21411-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/660b985e8e93/molecules-19-21411-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/0185dbc1247f/molecules-19-21411-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36dd/6270900/1e17bc36480c/molecules-19-21411-g007.jpg

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