赤芍总苷对人肝癌SMMC-7721细胞迁移的影响及作用机制探讨

杨玉; 王帅; 孟宪生; 包永睿

doi:10.13422/j.cnki.syfjx.2015060108

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赤芍总苷对人肝癌SMMC-7721细胞迁移的影响及作用机制探讨

药理 | 更新时间：2024-01-04

- 赤芍总苷对人肝癌SMMC-7721细胞迁移的影响及作用机制探讨
- Study on Migration of SMMC-7721 Hepatocarcinoma Cells Included by Total Paeony Glucosides and Its Preliminary Mechanism
- 中国实验方剂学杂志 2015年21卷第6期页码：108-112
- 作者机构：
- 作者简介：
- 基金信息：
  
  国家"重大新药创制"科技重大专项(2013ZX09507005)
- DOI：10.13422/j.cnki.syfjx.2015060108
  中图分类号： R285
- 纸质出版日期：2015
- 稿件说明：
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杨玉, 王帅, 孟宪生, 等. 赤芍总苷对人肝癌SMMC-7721细胞迁移的影响及作用机制探讨[J]. 中国实验方剂学杂志, 2015,21(6):108-112.

YANG Yu, WANG Shuai, MENG Xian-sheng, et al. Study on Migration of SMMC-7721 Hepatocarcinoma Cells Included by Total Paeony Glucosides and Its Preliminary Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(6): 108-112.
杨玉, 王帅, 孟宪生, 等. 赤芍总苷对人肝癌SMMC-7721细胞迁移的影响及作用机制探讨[J]. 中国实验方剂学杂志, 2015,21(6):108-112. DOI： 10.13422/j.cnki.syfjx.2015060108.

YANG Yu, WANG Shuai, MENG Xian-sheng, et al. Study on Migration of SMMC-7721 Hepatocarcinoma Cells Included by Total Paeony Glucosides and Its Preliminary Mechanism[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(6): 108-112. DOI： 10.13422/j.cnki.syfjx.2015060108.

摘要

目的: 探讨赤芍总苷对肝癌细胞SMMC-7721细胞迁移能力的影响及对血管内皮生长因子(VEGF)

环氧合酶-2(COX-2)表达的影响。方法: 体外培养SMMC-7721细胞

随机分组

不加药物作用的为空白组

其他各组为赤芍总苷低、中、高剂量组

将不同质量浓度(200

400

600 mg ·L-1)的赤芍总苷作用于细胞24 h后

采用MTT法检测赤芍总苷对细胞抑制作用

细胞划痕实验测定迁移能力

RT-PCR检测COX-2 mRNA表达

Western blot检测VEGF蛋白的表达。结果: 与空白组比较

赤芍总苷能够明显的抑制肝癌SMMC-7721细胞的增殖

且呈现量效关系(P<0.01)

并能够抑制细胞的迁移(P<0.01)

RT-PCR及Western blot结果显示

赤芍总苷作用细胞24 h后

可使COX-2 mRNA和VEGF蛋白的表达明显下降(P<0.01)。结论: 赤芍总苷能够抑制肝癌SMMC-7721细胞的生长、迁移

其机制可能是通过下调COX-2

VEGF的表达来实现

从而为赤芍总苷治疗肝癌的发展及其临床应用提供理论和实验依据。

Abstract

Objective: To investigate the migration of SMMC-7721 hepatocarcinoma cells induced by total paeony glucosides(TPG) and its impact on vascular endothelial growth factor (VEGF)

cyclooxygenase (COX) -2 expression. Method: SMMC-7721 cells were cultured with culture solution as blank group and TPG in different concentrations (200

400

600 mg · L-1) for 24 h in vitro. Inhibition on proliferation of cells was assessed by MTT assay. Cell migration was detected by wound scratch assay. COX-2 mRNA expression was detected by RT-PCR. VEGF protein expression was detected by Western blot. Result: Compared to the blank group

the proliferation of liver cancer SMMC-7721 cells were significantly inhibited by TPG in a concentration-dependent manner (P<0.05). The cell migration ability was inhibited (P<0.05)

the expression of COX-2 mRNA and VEGF protein decreased in the TPG groups. Conclusion: TPG could inhibit the growth and migration of liver cancer SMMC-7721 cells. Its mechanism may be realated to downregulating the expressions of COX-2 and VEGF. The fingdings provide theoretical and experimental basis for the development and clinical application of TGF in treating liver cancer.

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