Knockdown of PFKFB2 Alleviates Oxidative Stress and Inflammation in LPS-Induced Alveolar Epithelial Cells by Reducing Glycolysis

Abstract

Glycolysis is the most important mode of energy metabolism in endothelial cells and has been shown to be involved in the pathological processes of acute and chronic inflammatory diseases. Phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) exerts an important regulatory factor in the process of glycolysis by catalyzing the synthesis and degradation of fructose 2,6-bisphosphate. There is still unclear however, whether PFKFB2 can play a role in sepsis-related acute lung injury by regulating glycolysis. This research examines the role and mechanism of PFKFB2 in LPS-induced alveolar epithelial cells. In this study, the detection of mRNA expressions of PFKFB2, glycolysis and inflammation-related proteins employed quantitative real-time PCR (RTqPCR). Western blot was applied to examine the expressions of all proteins. The viability of A549 cells was assessed with the use of cell counting kit (CCK)-8. The expressions of related factors were quantified by commercial assay kits, respectively. The experimental results showed that the expression of PFKFB2 was increased in sepsis. Knockdown of PFKFB2 alleviated glycolysis in LPS-induced A549 cells. Additionally, knockdown of PFKFB2 reduced LPS-induced oxidative stress and inflammation through glycolysis. Knockdown of PFKFB2 also mitigated LPS-induced oxidative stress and inflammation in alveolar epithelial cells by reducing glycolysis. Hence, PFKFB2 may be served as an effective target for the treatment of sepsis-related acute lung injury.