Mechanism Investigation of Cell Cycle Arrest in Hepatic Cancer Cell Induced by Safflower Polysaccharide

SUN Yang; YANG Jing; ZHANG Qi-qi; WANG Xue; XU Fang; LI Ming-zhu; WANG Ya-xian

doi:10.13422/j.cnki.syfjx.2014130156

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Mechanism Investigation of Cell Cycle Arrest in Hepatic Cancer Cell Induced by Safflower Polysaccharide

更新时间：2024-01-04

- Mechanism Investigation of Cell Cycle Arrest in Hepatic Cancer Cell Induced by Safflower Polysaccharide
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 20, Issue 13, Pages: 156-159(2014)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2014130156
  CLC： R285
- Published：2014
- 稿件说明：
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SUN Yang, YANG Jing, ZHANG Qi-qi, et al. Mechanism Investigation of Cell Cycle Arrest in Hepatic Cancer Cell Induced by Safflower Polysaccharide[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(13): 156-159.
DOI：

SUN Yang, YANG Jing, ZHANG Qi-qi, et al. Mechanism Investigation of Cell Cycle Arrest in Hepatic Cancer Cell Induced by Safflower Polysaccharide[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(13): 156-159. DOI： 10.13422/j.cnki.syfjx.2014130156.

摘要

目的：通过研究红花多糖（safflower polysaccharide，SPS）对人肝癌SMMC-7721细胞增殖的影响，探讨SPS抗肿瘤作用的分子机制。方法：体外培养人肝癌SMMC-7721细胞，加入含不同质量浓度SPS（0，0.02，0.04，0.08，0.16，0.32，0.64，1.28 g·L-1）的培养液，分别培养24，48 h，用四甲基偶氮唑盐比色法（MTT法）检测SPS对细胞增殖的影响；用免疫组化法检测0.16，0.32，0.64 g·L-1SPS作用肝癌细胞48 h，细胞的细胞周期素B1（cyclin B1）蛋白表达；采用实时荧光定量PCR技术（realtime PCR，RT-PCR）和蛋白免疫印迹（Western blot）法检测细胞分裂周期25B（Cdc25B）基因的表达。结果：肝癌细胞的生存率随SPS浓度和作用时间的增加而降低，而1.28 g·L-1SPS组除外。SPS作用48 h后SMMC-7721细胞的cyclin B1蛋白、Cdc25B蛋白和mRNA表达降低，并具有剂量依赖性。结论： SPS可能通过抑制细胞周期相关基因的表达，诱导肝癌细胞增殖阻滞，进而起到抗肿瘤作用。

Abstract

Objective: To detect how safflower polysaccharide (SPS) affects cell proliferation of human hepatic cancer cell line SMMC-7721. Method: SMMC-7721 cells were treated with different concentrations(0

0.02

0.04

0.08

0.16

0.32

0.64

1.28 g·L-1) of SPS for 24

48 hours. The cell proliferation was assessed by methyl thiazolyl tetrazolium (MTT) assay. The proteins of cyclin B1 were compared by IHC. The expression of mRNA and protein of Cdc25B was compared by RT-PCR and Western blot. Result: The cell survival rate of SMMC-7721 cells was significantly inhibited by SPS in a dose-dependent and time-dependent manner

except 1.28 g·L-1 SPS group. The protein expression of cyclin B1 and Cdc25B was down-regulated compared with the control group at 48 hour. The mRNA of Cdc25B also decreased and had good dose-dependent. Conclusion: SPS can inhibit proliferation of SMMC-7721 cell by affecting expression of cycle regulation genes.

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