Astragalus polysaccharides inhibit the growth and proliferation of human hepatocellular carcinoma cell via AMPK-mTOR pathway

Abstract

Objective To investigate the effect of astragalus polysaccharides (APS) on the growth and proliferation of hepatocellular carcinoma cells and its effect on adenosine monophosphate activated protein kinase (AMPK) activity. Methods Hepatocellular carcinoma HepG2 cells cultured for 12, 24, and 48 hours were treated with 200, 300, and 400 mg/L concentration of astragalus polysaccharides. The cell inhibition rate was detected with methyl thiazolyl tetrazolium (MTT), and apoptosis was observed under the fluorescence microscope. Western blot method was used to measure the expression of total AMPK, phosphorylated AMPK (p-AMPK), and phosphorylate mammalian target of rapamycin (p-mTOR) protein expressions. Results Astragalus polysaccharides of each concentration significantly inhibited the proliferation of human hepatoma HepG2 cells (P<0.01), and the effect of 300 mg/L concentration astragalus polysaccharides was more significant than that of the 200 mg/L concentration (P<0.01); while inhibitory effect of 400 and 300 mg/L Astragalus polysaccharides on the proliferation of human hepatoma cell line HepG2 was not significant difference. We found that Astragalus polysaccharides of each concentration could promote the apoptosis of HepG2 cells, and the effect of 300 mg/L Astragalus polysaccharides was more significant. However, astragalus polysaccharide of 400 mg/L concentration could promote the apoptosis no more than the 300 mg/L concentration, which was observed by fluorescent microscope. Western blot results showed that astragalus polysaccharides could increase the expression of p-AMPK (P<0.05), and inhibit its downstream protein expressions of p-mTOR (P<0.05). The proliferation effect of astragalus polysaccharides was weakened after accession of AMPK antagonist compound C on hepatocellular carcinoma cells. Conclusions APS can inhibit the growth and proliferation of hepatocarcinoma cells, and its mechanism is related to the AMPK-mTOR pathway. Key words: ASTRAGALAN/PD; Liver neoplasms/DT/PP/ME; Cell proliferation/DE; Adenylate kinase/BI; Tacrolimus binding proteins/BI