Your browser doesn't support javascript.
loading
Ganoderma lucidum Polysaccharides Inhibit Malignant Phenotype of Hepatocellular Carcinoma Cells by Regulating PI3K/Akt Signaling Pathway / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae ; (24): 88-94, 2023.
Artículo en Chino | WPRIM | ID: wpr-961687
ABSTRACT
ObjectiveTo 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. MethodSK-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. ResultCompared with the blank group, the three doses of GLP reduced the proliferation and migration of SK­HEP­1 and Huh­7 cells (P<0.05), increased the percentage of cells in G1 phase (P<0.05), and decreased percentage of cells in S and G2 phase (P<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 (P<0.05). ConclusionGLP significantly inhibited the malignant phenotype of SK-HEP-1 and Huh-7 cells through the PI3K/Akt signaling pathway.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Experimental Traditional Medical Formulae Año: 2023 Tipo del documento: Artículo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Experimental Traditional Medical Formulae Año: 2023 Tipo del documento: Artículo