Antitumor activity of triptolide in SKOV3 cells and SKOV3/DDP in vivo and in vitro

Antitumor activity of triptolide in SKOV3 cells and SKOV3/DDP in vivo and in vitro
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雷公藤内酯醇在 SKOV3 细胞和 SKOV3/DDP 体内和体外的抗肿瘤活性。

DOI:
10.1097/cad.0000000000000894
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发表时间:
2020-06-01
期刊:
影响因子:
2.3
通讯作者:
Yang Lilan
Yang Lilan
中科院分区:
医学4区
文献类型:
--
作者:
Hu Hui;Zhu Sihong;Yang Lilan

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本研究旨在探讨雷公藤内酯醇对卵巢癌SKOV 3细胞和SKOV 3/顺铂(DDP)细胞的抗肿瘤作用及其机制。采用体内外实验研究雷公藤内酯醇对SKOV 3和SKOV 3/DDP细胞生长的影响。实验分为4组:SKOV 3组、SKOV 3 + TP组、SKOV 3/DDP组和SKOV 3/DDP + TP组。免疫印迹法和免疫组化法检测Sorcin、血管内皮生长因子和基质金属蛋白酶-2的表达。末端脱氧核苷酸转移酶dUTP缺口末端标记法检测肿瘤细胞凋亡。体外实验结果显示,与SKOV 3对照组相比,SKOV 3/DDP细胞集落刺激因子1水平和Sorcin表达明显升高。有趣的是,雷公藤内酯醇处理可以降低SKOV 3和SKOV 3/DDP细胞系中的集落刺激因子1水平和Sorcin表达。体内实验显示SKOV 3 + TP组和SKOV 3/DDP + TP组的组织坏死面积分别大于SKOV 3组和SKOV 3/DDP组。雷公藤内酯醇处理SKOV 3和SKOV 3/DDP细胞均诱导凋亡。与SKOV 3组相比,SKOV 3/DDP组肿瘤体积较大,MMP-2、Sorcin和血管内皮生长因子表达增高。雷公藤内酯醇治疗降低了SKOV 3/DDP和SKOV 3肿瘤的大小,并降低了MMP-2、Sorcin和血管内皮生长因子的表达。结论:雷公藤内酯醇对SKOV 3和SKOV 3/DDP细胞均有抗肿瘤作用,其作用机制可能与诱导细胞凋亡,调节MMP-2、Sorcin和VEGF的表达有关。
This study was designed to investigate the antitumor activity of triptolide in ovarian cancer inoculated with SKOV3 and SKOV3/cisplatin (DDP) cells, and to assess the mechanisms. In-vivo and in-vitro experiments were designed to evaluate the effects of triptolide on the tumor growth of SKOV3 and SKOV3/DDP cells. The experiments were divided into four groups: a SKOV3 group, a SKOV3 + TP treatment group, a SKOV3/DDP group and a SKOV3/DDP + TP treatment group. The expression of Sorcin, vascular endothelial growth factor and matrix metalloproteinase-2 were detected by western blotting and immunohistochemistry. Tumor cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling. In-vitro experiments showed that compared with SKOV3 control group, the level of colony-stimulating factor 1 and expression of Sorcin in SKOV3/DDP was significantly higher. Interestingly, triptolide treatment could reduce colony-stimulating factor 1 level and expression of Sorcin in both SKOV3 and SKOV3/DDP cell lines. In-vivo experiments showed that tissue necrosis area in SKOV3 + TP and SKOV3/DDP + TP was larger than SKOV3 and SKOV3/DDP group, respectively. Triptolide treatment induced apoptosis in both SKOV3 and SKOV3/DDP cells. Compared with SKOV3 group, the size of tumors was large, and the expression of MMP-2, Sorcin and vascular endothelial growth factor was higher in SKOV3/DDP group. Triptolide treatment reduced the size of tumors, and the expression of MMP-2, Sorcin and vascular endothelial growth factor in SKOV3/DDP as well as in SKOV3 tumors. In conclusion, triptolide has antitumor activity in both SKOV3 and SKOV3/DDP cells likely through inducing apoptosis and regulating MMP-2, Sorcin and vascular endothelial growth factor expression.