Hepatic
fibrosis is defined as a pathological process, and activation of hepatic stellate cells (HSCs) is believed to be the key event of
liver fibrosis. Additionally, activated HSCs may participate in the formation of the tumor microenvironment.
Polaprezinc, a protector of the gastric mucosa, has been recently demonstrated to be an inhibitor of
liver fibrosis in a mouse model. Proliferation and colony formation assays were performed to determine the inhibitory effects of
polaprezinc on the growth of LX‑2 and hepG2 cells. A migration assay was used to evaluate the change in mobility of LX‑2 cells and quantitative polymerase chain reaction was performed to detect the expression levels of key markers of
fibrosis. Finally, a gene chip assay for polaprezinc‑treated hepG2 cells was performed to evaluate the effect of
polaprezinc on the hepG2 gene expression profile. The proliferation assay indicated that
polaprezinc may inhibit the LX‑2 cell proliferation and the migration assays confirmed the inhibition of mobility. The expression levels of fibrotic markers such as
collagen I,
fibronectin and α‑smooth muscle actin were downregulated following
polaprezinc treatment. The proliferation activity of polaprezinc‑treated hepG2 cells was reduced and the gene chip assay indicated that series of gene expression changes associated with
cancer migration, cell skeletal organization and proliferation had occurred. In conclusion,
polaprezinc treatment mayinhibit the proliferation of
hepatocellular carcinoma cells and reverse
liver fibrosis by deactivating HSCs. The present findings suggest that
polaprezinc provides a novel treatment for patients with
gastritis complicated with
cirrhosis.