<italic style="font-style: italic">Ganoderma lucidum</italic> Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway

SHEN Rui; XU Jing; WANG Lei; CAI Biao; SONG Hang

doi:10.13422/j.cnki.syfjx.2022002023

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Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway

更新时间：2023-02-15

- Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 29, Issue 6, Pages: 88-94(2023)
- 作者机构：
  
  安徽中医药大学，合肥 230012
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2022002023
  CLC： R22;R242;R2-031;R285.5
- Published：20 March 2023，
  
  Published Online：18 August 2022，
  
  Received：29 March 2022，
- 稿件说明：
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沈瑞,徐静,王雷等.灵芝多糖调控PI3K/Akt信号通路抑制肝癌细胞恶性表型[J].中国实验方剂学杂志,2023,29(06):88-94.

SHEN Rui,XU Jing,WANG Lei,et al.Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2023,29(06):88-94.
沈瑞,徐静,王雷等.灵芝多糖调控PI3K/Akt信号通路抑制肝癌细胞恶性表型[J].中国实验方剂学杂志,2023,29(06):88-94. DOI： 10.13422/j.cnki.syfjx.2022002023.

SHEN Rui,XU Jing,WANG Lei,et al.Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway[J].Chinese Journal of Experimental Traditional Medical Formulae,2023,29(06):88-94. DOI： 10.13422/j.cnki.syfjx.2022002023.

摘要

目的

观察灵芝多糖对肝癌细胞SK-HEP-1和Huh-7增殖、迁移、细胞周期及凋亡的影响，同时探讨其可能的作用机制。

方法

将肝癌细胞SK-HEP-1和Huh-7作为主要研究对象，设立空白组和灵芝多糖低、中、高组（3.5、7、14 g·L

-1

）。细胞增殖与活性检测-8（CCK-8）法检测灵芝多糖对肝癌细胞增殖能力的影响；划痕实验检测灵芝多糖对肝癌细胞迁移能力的影响；流式细胞术测定灵芝多糖对肝癌细胞周期的影响；Hoechst33258染色法测定灵芝多糖对肝癌细胞凋亡的影响，通过蛋白免疫印迹法检测灵芝多糖对肝癌细胞磷脂酰肌醇3-激酶（PI3K）、蛋白激酶B（Akt）、磷酸化PI3K（p-PI3K）、磷酸化Akt（p-Akt）蛋白表达水平的影响。

结果

与空白组比较，灵芝多糖低、中、高组SK-HEP-1和Huh-7细胞增殖和迁移能力降低（

0.05）；灵芝多糖低、中、高组G

期细胞比例升高（

0.05），S期和G

期细胞比例降低（

0.05）；灵芝多糖低、中、高组可以诱导2种肝癌细胞凋亡，并且药物浓度越高作用越明显。与空白组比较，灵芝多糖低、中、高组PI3K和Akt的磷酸化水平降低（

0.05）。

结论

灵芝多糖对肝癌细胞SK-HEP-1和Huh-7的恶性表型有显著抑制作用，其作用机制与PI3K/Akt信号通路有关。

Abstract

Objective

To investigate the effect of

Ganoderma lucidum

polysaccharides （GLP） on the proliferation， migration， cycle， and apoptosis of hepatocellular carcinoma SKHEP1 and Huh7 cells and to explore the underlying mechanism.

Method

SK-HEP-1 and Huh-7 cells were classified into the blank group and low-， medium-， and high-dose GLP groups （3.5， 7， 14 g·L

-1

）. The proliferation of the cells was examined by cell counting kit-8 （CCK8） assay， and the migration by scratch assay. Cell cycle was measured by flow cytometry and apoptosis was detected based on Hoechst33258 staining. In addition， the expression of phosphatidylinositol 3-kinase （PI3K）， protein kinase B （Akt）， phosphorylated PI3K （pPI3K）， and phosphorylated Akt （pAkt） in the cells was determined by Western blot.

Result

Compared with the blank group， the three doses of GLP reduced the proliferation and migration of SKHEP1 and Huh7 cells （

0.05）， increased the percentage of cells in G

phase （

0.05）， and decreased percentage of cells in S and G

phase （

0.05）. In addition， the three doses can induce apoptosis of both SK-HEP-1 and Huh-7 cells， particularly the high dose. Moreover， the three doses of GLP lowered the levels of pPI3K and pAkt （

0.05）.

Conclusion

GLP significantly inhibited the malignant phenotype of SK-HEP-1 and Huh-7 cells through the PI3K/Akt signaling pathway.

关键词

灵芝多糖肝癌细胞实验恶性表型磷脂酰肌醇3激酶/蛋白激酶B （PI3K/Akt）信号通路

Keywords

Ganoderma lucidum polysaccharidesliver cancercell experimentmalignant phenotypephosphatidylinositol3 kinase/protein kinase B （PI3K/Akt） signaling pathway

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Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway

DOI：10.13422/j.cnki.syfjx.2022002023

摘要

Abstract

关键词

Keywords

references