Inhibition Of Lncrna Hulc Improves Hepatic Fibrosis And Hepatocyte Apoptosis By Inhibiting The Mapk Signaling Pathway In Rats With Nonalcoholic Fatty Liver Disease

This study is conducted to investigate the role of long noncoding RNA highly upregulated in liver cancer (lncRNA HULC) on hepatic fibrosis and hepatocyte apoptosis by inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway in rats with nonalcoholic fatty liver disease (NAFLD). The successfully modeled rats were injected with HULC siRNA or small interfering RNA (siRNA) negative control into the tail vein. The expression of HULC in liver tissues was detected by reverse transcription quantitative polymerase reaction chain. The role of HULC in pathological state and liver function-related indexes of liver lipid deposition, the degree of hepatic fibrosis and hepatocyte apoptosis in rats with NAFLD were also investigated through a series of experiments. Increased expression of HULC was found in liver tissue of NAFLD rats. Inhibition of HULC improved the pathological state and liver function-related indexes of liver lipid deposition, improved the degree of hepatic fibrosis, reduced hepatocyte apoptosis, and inhibited the MAPK signaling pathway in the liver tissue of NAFLD rats. The inhibition of p38 and JNK improved the pathological state of liver lipid deposition and liver function to some extent, improved the degree of hepatic fibrosis, and reduced the apoptosis of hepatocytes in NAFLD rats. Collectively, this present study provides evidence that inhibition of lncRNA HULC improves hepatic fibrosis and decrease hepatocyte apoptosis in rats with NAFLD by inhibiting the MAPK signaling pathway.