[1]汤兆奇,王克生,徐宏彬,等.没药甾酮下调PI3K/Akt通路增强替莫唑胺抗脑胶质瘤细胞增殖作用[J].中国药理学通报,2019,(08):1098-1103.[doi:10.3969/j.issn.1001-1978.2019.08.013]
 TANG Zhao-qi,WANG Ke-sheng,XU Hong-bin,et al.Guggulsterone enhanced inhibitory effect of temozolomide on glioblastoma cells through PI3K/Akt pathway[J].Chinese Pharmacological Bulletin,2019,(08):1098-1103.[doi:10.3969/j.issn.1001-1978.2019.08.013]
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没药甾酮下调PI3K/Akt通路增强替莫唑胺抗脑胶质瘤细胞增殖作用()
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《中国药理学通报》[ISSN:/CN:]

卷:
期数:
2019年08期
页码:
1098-1103
栏目:
论著
出版日期:
2019-08-14

文章信息/Info

Title:
Guggulsterone enhanced inhibitory effect of temozolomide on glioblastoma cells through PI3K/Akt pathway
文章编号:
1001-1978(2019)08-1098-06
作者:
汤兆奇1王克生2徐宏彬1 3 4
1.南京医科大学上海十院临床医学院,江苏 南京 211166; 2.上海市第十人民医院中心实验室,上海 200072; 3.上海市第十人民医院药学部,上海 200072; 4.上海市第十人民医院崇明分院药剂科,上海 202157
Author(s):
TANG Zhao-qi1 WANG Ke-sheng2 XU Hong-bin1 3 4
1.Clinical Medical College of Shanghai Tenth People's Hospital, Nanjing Medical University, Nanjing 211166, China; 2.Central Lab, Shanghai Tenth People's Hospital, Shanghai 200072, China; 3.Dept of Pharmacy, Shanghai Tenth People's Hospital,Shanghai 200072, China; 4.Dept of Pharmacy,Chongming Branch of Shanghai Tenth People's Hospital, Shanghai 202157, China
关键词:
没药甾酮 脑胶质瘤 替莫唑胺 增殖 凋亡 机制
Keywords:
guggulsterone glioblastoma temozolomide proliferation apoptosis mechanism
分类号:
R282.71; R329.24; R329.25; R730.264; R739.41; R916.4
DOI:
10.3969/j.issn.1001-1978.2019.08.013
文献标志码:
A
摘要:
目的 探讨没药甾酮增强替莫唑胺抗人脑胶质瘤细胞增殖的作用及机制。方法 分别用CCK-8、Hoechst 33342染色和流式细胞术、Western blot检测没药甾酮、替莫唑胺单药及联合对人脑胶质瘤U251细胞增殖、凋亡、PI3K/Akt通路活性,以及凋亡相关蛋白Bcl-2、Bax表达影响。结果 与替莫唑胺(1~400 μmol·L-1)单药组相比,没药甾酮(30 μmol·L-1)联合替莫唑胺(1~400 μmol·L-1)明显增强对人脑胶质瘤U251细胞的抗增殖作用; 与替莫唑胺(400 μmol·L-1)单药组相比,没药甾酮(30 μmol·L-1)联合替莫唑胺(400 μmol·L-1)明显增强对人脑胶质瘤U251细胞的凋亡诱导作用(P<0.01); 与替莫唑胺(400 μmol·L-1)单药组相比,没药甾酮(30 μmol·L-1)联合替莫唑胺(400 μmol·L-1)明显下调PI3K、p-PI3K p110、p-Akt(Ser473)和Bcl-2的表达。结论 没药甾酮可通过下调PI3K/Akt通路,增强替莫唑胺对人脑胶质瘤细胞U251的增殖抑制作用。
Abstract:
Aim To investigate the mechanism of the combination of guggulsterone and temozolomide in inhibiting human glioblastoma cells.Methods Glioblastoma U251 cells were treated with guggulsterone and temozolomide alone or in combination.Cell proliferation was determined by CCK-8.The level of apoptosis was evaluated by Hoechst 33342 staining and flow cytometry.PI3K/Akt pathway activity and the level of apoptosis-associated proteins Bcl-2 and Bax expression were analysed by Western blot.Results Guggulsterone(30 μmol·L-1)significantly enhanced the inhibitory effect of temozolomide(1~400 μmol·L-1)on U251 cells, as compared with temozolomide treatment alone.Guggulsterone(30 μmol·L-1)significantly enhanced the effect of temozolomide(400 μmol·L-1)-induced apoptosis on U251 cells, as compared with temozolomide treatment alone(P<0.01).Furthermore, guggulsterone(30 μmol·L-1)significantly down-regulated the expression of PI3K, p-PI3K p110, p-Akt(Ser473)and Bcl-2, as compared with temozolomide treatment alone.Conclusion Guggulsterone enhances the inhibitory effect of temozolomide on human glioblastoma U251 cells through PI3K/Akt pathway.

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备注/Memo

备注/Memo:
收稿日期:2019-04-16,修回日期:2019-05-20
基金项目:上海市崇明区科委“可持续发展科技创新行动计划”项目(No CKY2018-25)
作者简介:汤兆奇(1992-),男,硕士生,研究方向:肿瘤药理学,E-mail: 1095339046@qq.com;
徐宏彬(1972-),男,博士,主任药师,博士生导师,研究方向:肿瘤药理学,通讯作者,Tel: 021-66302761,E-mail: xuhongbin@tongji.edu.cn
更新日期/Last Update: 2019-08-14