TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000379775
  • Gene Name:PFKFB3
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:Dehydrocostus lactone
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:acute lung injury
  • Tissue:

Other information

  • Title:Dehydrocostus Lactone Ameliorates LPS-Induced Acute Lung Injury by Inhibiting PFKFB3-Mediated Glycolysis
  • Journal:Journal of Cellular Biochemistry
  • Published:2024
  • PubMed ID:39148265
  • Abstract:Acute lung injury (ALI) is a destructive respiratory disease characterized by alveolar structural destruction and excessive inflammation responses. Aerobic glycolysis of macrophages plays a crucial role in the pathophysiology of ALI. Previous studies have shown that the expression of the key rate-limiting enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in inflammatory cells is significantly increased, which promotes an increase in the rate of glycolysis in inflammatory cells. However, little is known about the biological functions of PFKFB3 in macrophage inflammation and ALI. In this study, we identified that PFKFB3 is markedly increased in lipopolysaccharide (LPS)-induced ALI mice and macrophages. Knockdown of pfkfb3 attenuated LPS-induced glycolytic flux, decreased the release of pro-inflammatory cytokines, and inactivated NF-κB signaling pathway in macrophages. Subsequently, we found that dehydrocostus lactone (DL), a natural sesquiterpene lactone, significantly decreased both the mRNA and protein levels of PFKFB3. Furthermore, it reduced the release of inflammatory cytokines and inactivated NF-κB pathways in vitro. Accordingly, DL alleviated LPS-induced pulmonary edema and reduced the infiltration of inflammatory cells in mouse lung tissue. In summary, our study reveals the vital role of PFKFB3 in LPS-induced inflammation and discovers a novel molecular mechanism underlying DL＇s protective effects on ALI.
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