[No authors listed]
Acute liver failure (ALF) is a fatal liver disease characterized by severe hepatocyte destruction. MicroRNAs (miRNAs/miRs) have been reported to serve a key role in a number of liver diseases. Therefore, the aim of the present study was to investigate the role and underlying mechanism of miRâ214 in ALF. ALF murine and hepatocyte models were established using Dâgalactosamine (DâGalN) and lipopolysaccharide (LPS) or DâGalN + tumor necrosis factor (TNF)âα, respectively. The expression levels of miRâ214 and Bax were detected by reverse transcriptionâquantitative polymerase chain reaction (RTâqPCR) and/or western blotting. Furthermore, an automatic biochemical analyzer was used to measure the levels of aspartate aminotransferase (AST) or alanine aminotransferase (ALT). The levels of TNFâα and interleukin (IL)â6 were detected by ELISA and RTâqPCR. In addition, TUNEL staining and flow cytometry were used to analyze cell apoptosis, and the protein expression of caspaseâ3 was determined by western blotting. It was identified that the levels of AST and ALT were increased and that hepatocyte apoptosis was enhanced in the DâGalN/LPSâstimulated group compared with the control. Furthermore, higher expression of caspaseâ3 was observed in the DâGalN/LPSâstimulated group. In addition, it was demonstrated that miRâ214 was downregulated, while Bax was upregulated in DâGalN/LPSâstimulated mice and DâGalN/TNFâαâstimulated BNLCL2 cells. Moreover, in DâGalN/TNFâαâstimulated BNLCL2 cells, miRâ214 overexpression suppressed apoptosis and decreased TNFâα and ILâ6 levels, and these effects were reversed by the Bax plasmid. It was also identified that overexpression of miRâ214 significantly decreased Bax mRNA and protein expression levels in vitro. Collectively, the present results suggested that miRâ214 inhibited hepatocyte apoptosis during ALF development via targeting Bax, thus indicating that miRâ214 may be a potential target for ALF treatment.
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