The Role of miR-150-5p/SOCS1 Pathway in Arsenic-Induced Pyroptosis of LX-2 Cells.

This study aims to explore the mechanism of pyroptosis of human hepatocyte LX-2 cells induced by NaAsO₂ through the miR-150-5p/SOCS1 pathway. LX-2 cells were transfected with different concentrations of NaAsO₂, miR-150-5p inhibitor, and SOCS1 agonist. Cell activity, cell pyroptosis, and the expression of related genes and proteins were detected by scanning electron microscopy, CCK-8, qRT-PCR, western blot, and immunofluorescence. Compared with the control group, 10 µmol/L and 20 µmol/L NaAsO₂ significantly elevated the protein expression levels of the pyroptosis-related proteins NLRP3, GSDMD, GSDMD-N, caspase1, and cleaved caspase1 as well as the mRNA levels of NLRP3, GSDMD, caspase1, IL-18, and IL-1β. The typical pyroptosis with swelling and rupture of the plasma membrane was observed through scanning electron microscopy. The expression of miR-150-5p of the NaAsO₂ intervention group increased, while the expression of SOCS1 decreased; then the level of NF-κB p65 elevated. With co-treatment of miR-150-5p inhibitor, SOCS1 agonist, and NaAsO₂, the cell pyroptosis was attenuated, and the expressions of NLRP3, caspase1, GSDMD, GSDMD-N, IL-18, IL-1β, p65 of the group of miR-150-5p inhibitor and NaAsO₂ group, and of the group of SOCS1 agonist and NaAsO₂ reduced compared with the NaAsO₂ group. Arsenic exposure promotes miR-150-5p, inhibits the expression of SOCS1, and activates the NF-κB/NLRP3 pathway in LX-2 cell pyroptosis.