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薯蓣皂苷通过调节VEGFR2和PI3K/AKT/MAPK信号通路抑制卵巢癌细胞的活力。

Dioscin suppresses the viability of ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways.

作者信息

Guo Xianqing, Ding Xiao

机构信息

Department of Pharmaceuticals, Qilu Hospital of Shandong University, Qingdao, Shandong 266035, P.R. China.

Department of Gynecology and Obstetrics, Qilu Hospital of Shandong University, Qingdao, Shandong 266035, P.R. China.

出版信息

Oncol Lett. 2018 Jun;15(6):9537-9542. doi: 10.3892/ol.2018.8454. Epub 2018 Apr 10.

DOI:10.3892/ol.2018.8454
PMID:29805675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5958686/
Abstract

Diosgenin is a natural steroidal saponin that is extracted from a range of sources, including from fenugreek. It is a critical raw material in the synthesis of steroid hormone drugs, exhibiting antitumor, anti-inflammatory, antioxidation and a number of other significant pharmacological actions, possessing high pharmaceutical value. The aim of the present study was to investigate the effects of dioscin suppression on ovarian cancer cell growth and the mechanism of apoptosis induction by dioscin in ovarian cancer cells. The results of the present study demonstrated that dioscin decreased viability and induced apoptosis in SKOV3 human ovarian cancer cells in a dose-dependent manner. Dioscin significantly increased caspase-3 and caspase-9 activity, and increased the protein expression of Bax and cleaved poly(ADP-ribose) polymerase in SKOV3 cells. In addition, dioscin significantly suppressed vascular endothelial growth factor receptor (VEGFR)2, phosphoinositide 3-kinase (PI3K), phosphorylated AKT and phosphorylated p38 mitogen-activated protein kinase (MAPK) protein expression in SKOV3 cells. Taken together, to the best of our knowledge, the present study demonstrated for the first time that dioscin suppresses cell viability in ovarian cancer cells by regulating the VEGFR2 and PI3K/AKT/MAPK signaling pathways.

摘要

薯蓣皂苷元是一种天然甾体皂苷,可从包括胡芦巴在内的多种来源中提取。它是合成甾体激素药物的关键原料,具有抗肿瘤、抗炎、抗氧化等多种重要药理作用,具有很高的药用价值。本研究的目的是探讨薯蓣皂苷抑制卵巢癌细胞生长的作用及其诱导卵巢癌细胞凋亡的机制。本研究结果表明,薯蓣皂苷以剂量依赖的方式降低SKOV3人卵巢癌细胞的活力并诱导其凋亡。薯蓣皂苷显著增加SKOV3细胞中caspase-3和caspase-9的活性,并增加Bax和裂解的聚(ADP-核糖)聚合酶的蛋白表达。此外,薯蓣皂苷显著抑制SKOV3细胞中血管内皮生长因子受体(VEGFR)2、磷酸肌醇3-激酶(PI3K)、磷酸化AKT和磷酸化p38丝裂原活化蛋白激酶(MAPK)的蛋白表达。综上所述,据我们所知,本研究首次证明薯蓣皂苷通过调节VEGFR2和PI3K/AKT/MAPK信号通路抑制卵巢癌细胞的活力。

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