Galectin-1 gene silencing inhibits the activation and proliferation but induces the apoptosis of hepatic stellate cells from mice with liver fibrosis.

Abstract

Liver fibrosis is a serious threat to human health, and there is currently no effective clinical drug for treatment of the disease. Although Galectin-1 is effective, its role in liver function, inflammation, matrix metalloproteinases and the activation of hepatic stellate cells (HSCs) remains to be elucidated. The aim of the present study was to elucidate the effect of Galectin-1 on the activation, proliferation and apoptosis of HSCs in a mouse model of liver fibrosis. Following successful model establishment and tissue collection, mouse HSCs (mHSCs) were identified and an mHSC line was constructed. Subsequently, to determine the role of Galectin-1 in liver fibrosis, the expression levels of transforming growth factor (TGF)-β1, connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) pre- and post-transfection were evaluated by reverse transcription-quantitative polymerase chain reaction and western blot analyses. In addition, the effects of Galectin-1 on the biological behavior and mitochondrial function of mHSCs were determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry and a scratch test. It was first observed that the expression levels of Galectin-1, TGF-β1, CTGF and α-SMA were downregulated by silencing the gene expression of Galectin-1. Additionally, silencing the gene expression of Galectin-1 inhibited cell cycle progression, proliferation and migration but induced the apoptosis of mHSCs from mice with liver fibrosis. Furthermore, the in vivo experimental results suggested that silencing the gene expression of Galectin-1 improved liver fibrosis. Collectively, it was concluded that silencing the gene expression of Galectin-1 ameliorates liver fibrosis and that functionally suppressing Galectin-1 may be a future therapeutic strategy for liver fibrosis.