Study Of Porphyromonas Gingivalis Promotes Glycolysis And Inflammatory Response Of Vascular Endothelial Cells Through HIF-1α

Objective: Porphyromonas gingivalis(P.gingivalis),the main pathogen causing periodontitis,has been shown to promote the inflammatory response of vascular endothelial cells and accelerate the occurrence and development of atherosclerosis.In this study,the effects of P.gingivalis on glycolysis and inflammation of vascular endothelial cells were analyzed.The role of hypoxia inducible factor 1α(HIF-1α)was also investigated.Materials: Firstly,they were divided into blank control group,P.gingivalis W83 group and P.gingivalis ATCC 33277 group.Glucose uptake levels of vascular endothelial cells were analyzed by fluorescence staining.Lactate production was measured by colorimetric assay.The protein expression of the key glycolysis enzymes 6-phosphofructo2-kinase/fructo2-kina-se/fructose-2,bisphosphatase3(PFKFB3)was determined by Western blot.These results indicate the level of cellular glycolysis.The protein expression of HIF-1α,Casein Kinase2-Interacting Protein1(CKIP-1)and Interleukin-6(IL-6)was measured by Western blot to determine the level of cellular inflammation.Subsequently,si RNA transfection silenced HIF-1α expression,and HIF-1α inhibitory agent YC-1 was used to explore the role of HIF-1α in P.gingivalis-induced glycolysis and inflammation.The experimental data were analyzed by SPSS20.0,and the results were expressed as mean ± standard deviation.P <0.05 was considered statistically significant.Results: 1.P.gingivalis infection significantly up-regulated the expression of HIF-1α(P<0.05).2.Glucose uptake,lactate production,and PFKFB3 protein expression of vascular endothelial cells increased after infection(P<0.05).3.P.gingivalis-induced inflammatory response showed decreased expression of CKIP-1 and increased expression of IL-6(P <0.05).4.HIF-1α silencing and YC-1 blocked the increased glycolysis and inflammatory response associated with P.gingivalis infection(P<0.05).Conclusions: HIF-1α is involved in increased glycolysis and inflammation of vascular endothelial cells induced by P.gingivalis infection.The results indicate the possible mechanism of vascular endothelial cell inflammation induced by P.gingivalis infection from the perspective of HIF-1α.This may be a therapeutic target for vascular endothelial cell injury caused by periodontitis.