番泻苷B抑制STAT3和ERK1/2磷酸化对A549细胞生长侵袭及裸鼠成瘤的影响

中国临床解剖学杂志 ›› 2019, Vol. 37 ›› Issue (6): 662-667.

番泻苷B抑制STAT3和ERK1/2磷酸化对A549细胞生长侵袭及裸鼠成瘤的影响

王俊杰¹，　段仁慧¹，　刘玲²

新乡市中心医院 1.肿瘤内三科； 2.检验科，河南新乡 453000

收稿日期:2019-01-25 出版日期:2019-11-25 发布日期:2019-12-02
作者简介:王俊杰（1985-），女，硕士，主治医师，研究方向：肿瘤内科，E-mail：xiangyue479086@sina.com
基金资助:
河南省科技发展计划（152300410163）

Effects of sennoside B on growth and invasion of A549 cells and tumorigenesis of nude mice by inhibiting the phosphorylation of STAT3 and ERK1/2

WANG Jun-jie¹, DUAN Ren-hui¹, LIU Ling²

Xinxiang Central Hospital, 1.Department of Three Families in Tumor; 2.Department of Clinical Laboratory, Xinxiang 453000, Henan Province, China

Received:2019-01-25 Online:2019-11-25 Published:2019-12-02

摘要/Abstract

摘要： 目的　探讨番泻苷B对A549细胞生长、侵袭及裸鼠成瘤的影响及机制。方法　采用0、5、10、20 μM番泻苷B处理非小细胞肺癌A549细胞，将细胞随机分为4组进行后续实验，Brdu染色检测各组细胞增殖；Hoechst染色检测细胞凋亡；划痕实验检测细胞迁移；Transwell实验检测细胞侵袭；蛋白免疫印迹检测ki67、PCNA 、cl-caspase-3、cl-caspase-9、VEGF、N-cadherin和E-cadherin蛋白表达水平，STAT3和ERK1/2的磷酸化情况;建立荷瘤小鼠模型，检测肿瘤重量，免疫组化检测Ki67和VEGF表达。结果　与Control组相比较，各番泻苷B剂量组Brdu阳性细胞数量、侵袭细胞数明显减少（P<0.05），细胞凋亡率明显上升（P<0.05），细胞划痕愈合率降低（P<0.05），ki67、PCNA、VEGF、N-cadherin蛋白水平明显降低（P<0.05），cl-caspase-3、cl-caspase-9、E-cadherin蛋白水平明显升高（P<0.05），STAT3和ERK1/2的磷酸化水平均明显降低（P<0.05），降低荷瘤小鼠肿瘤重量与Ki67和VEGF表达水平（P<0.05）。结论　番泻苷B抑制STAT3、ERK1/2磷酸化对A549细胞体内外生长有抑制作用。

关键词: 非小细胞肺癌, 　番泻苷B, 　STAT3, 　ERK1/2

Abstract: Objective　To investigate the effects and mechanisms of sennoside B on the growth, invasion of A549 cells and tumorigenesis of nude mice.　Methods　A549 non-small cell lung cancer cells were treated with sennoside B at doses of 0, 5, 10 and 20 μM respectively. The cells were divided into four groups randomly according to the dose and then the follow-up experiment was proceeded. Brdu staining was used to detect the cell proliferation of each group, and Hoechst staining was used to detect apoptosis. Cell migration was detected by scratch test. Cell invasion was detected by Transwell assay. Protein expression levels of Ki67, PCNA, cl-caspase-3, cl-caspase-9, VEGF, N-cadherin and E-cadherin, as well as phosphorylation of STAT3 and ERK1/2 were detected by western blotting. Tumor-bearing mice model was established and the weight of tumor was tested. The expression of Ki67 and VEGF were detected by immunohistochemistry.　Results　Compared with the Control group, the result showed that the Brdu positive cells number, the invasion cells number in each sennoside B dosage group were significantly reduced（P<0.05）, the apoptosis rate increased significantly（P<0.05）, the rate of cells scratches healing（P<0.05）, the protein levels of ki67, PCNA and VEGF, N-cadherin decreased obviously（P<0.05）, the protein levels of cl-caspase-3, cl-caspase-9, E-cadherin increased significantly（P<0.05）, phosphorylation levels of STAT3 and ERK1/2 were significantly reduced （P<0.05）, and the weight of tumor and the expression levels of Ki67 and VEGF were decreased in tumor-bearing mice model（P<0.05）.　Conclusions　Sennoside B inhibits the phosphorylation of STAT3 and ERK1/2 and the growth of A549 cells.

Key words: Non-small cell lung cancer, 　Sennoside B;　STAT3, 　ERK1/2

中图分类号:

R734.2

王俊杰, 段仁慧, 刘玲. 番泻苷B抑制STAT3和ERK1/2磷酸化对A549细胞生长侵袭及裸鼠成瘤的影响[J]. 中国临床解剖学杂志, 2019, 37(6): 662-667.

WANG Jun-jie, DUAN Ren-hui, LIU Ling. Effects of sennoside B on growth and invasion of A549 cells and tumorigenesis of nude mice by inhibiting the phosphorylation of STAT3 and ERK1/2[J]. Chinese Journal of Clinical Anatomy, 2019, 37(6): 662-667.

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