Selenoprotein X Gene Knockdown Aggravated H 2 O 2 -Induced Apoptosis in Liver LO2 Cells

Abstract

To determine the roles of selenoprotein X gene (Selx) in protecting liver cells against oxidative damage, the influences of Selx knockdown on H₂O₂-induced apoptosis in human normal hepatocyte (LO2) cells were studied. pSilencer 3.1 was used to develop knockdown vector targeting the 3′-UTR of human Selx. The Selx knockdown and control cells were further exposed to H₂O₂, and cell viability, cell apoptosis rate, and the expression levels of mRNA and protein of apoptosis-related genes were detected. The results showed that vector targeting the 3′-UTR of Selx successfully silenced mRNA or protein expression of SelX in LO2 cells. Selx knockdown resulted in decreased cell viability, increased percentage of early apoptotic cells, decreased Bcl2A1 and Bcl-2 expression, and increased phosphorylation of P38 in LO2 cells. When Selx knockdown LO2 cells were exposed to H₂O₂, characteristics of H₂O₂-induced cell dysfunctions were further exacerbated. Taken together, our findings suggested that SelX played important roles in protecting LO2 cells against oxidative damage and reducing H₂O₂-induced apoptosis in liver cells.

from Cancer via ola Kala on Inoreader http://ift.tt/2b7YZ3W
via IFTTT