Objective: To investigate the effect of aloe-emodin on the growth

migration and fibrous actin (F-actin) of hepatoma HepG2 cells. Method: The maximum toxic concentration (TC0) of aloe-emodin on human normal hepatocytes was screened out in the drug toxicity experiment for human normal hepatocyte cell line QSG-7701.TC0 was taken as the highest concentration

diluted to 3 different concentrations of aloe-emodin

and used to treat human hepatoma HepG2 cells in vitro for the aloe-emodin group; another untreated HepG2 cells were set up as a blank group; cell proliferation inhibition rate was measured by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay after 48 hours. Cell migration assay and scratch assay were used to detect the cell migration in both groups. The effect of aloe-emodin on the expression of HepG2 cell F-actin was analyzed by high-content cell imaging system. The expressions of phosphorylated endothelial nitric oxide synthase (p-eNOS) and nuclear transcription factor-κB p65 (NF-κB p65) in HepG2 cells were detected by Western blot. Result: TC0 of aloe-emodin on human normal hepatocyte cell line QSG-7701 was 50 μmol·L-1. TC0 was taken as the highest concentration to treat HepG2 cells with aloe-emodin (10

30

50 μmol·L-1). Compared with blank group

The proliferation inhibition rate of aloe-emodin group increased after 48 hours of culture

indicating the dose escalation thpe (P<0.01)

after 48 hours of culture

the scratch distance of aloe-emodin group was broadened

and the migrating ability of aloe-emodin group was decreased

indicating the dose decline type (P<0.01); F-actin area was shorten

disordered

irregular and fuzzy

indicating the dose decline type (P<0.01); the expression of NF-κB p65 in aloe-emodin group was increased

while the expression of p-eNOS was decreased

indicating the dose decline type (P<0.01). Conclusion: Aloe-emodin may reduce the proliferation and migration of HepG2 cells by increasing NF-κB p65

inhibiting the expression of p-eNOS

promoting the depolymerization of F-actin

and reducing the formation of microfilaments

with an effect in inhibiting tumor.