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Updated: Jul 17, 2026
Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
Published on: September 15, 2017
Bioinformatic Analysis and Experimental Verification Reveal the Protective Role of Baicalein Against LPS-Induced
Fuping Luo1, Jinxi Ao1, Yuan Chen1
1Department of Emergency Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan, 637000, People's Republic of China.
Background:
Endothelial cells play a central role in the pathogenesis of sepsis. Currently, effective therapeutic options for sepsis remain limited. Baicalein (BAI) is a compound with multiple bioactivities. This study aims to investigate the protective effects of BAI against lipopolysaccharide (LPS)-induced endothelial cell injury and to explore the underlying molecular mechanisms.
Methods:
Bioinformatics tools, including RNA sequencing (RNA-seq), immune cell infiltration analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, were utilized to explore the molecular mechanisms of BAI in human umbilical vein endothelial cells (HUVECs) induced by LPS. The LPS-induced HUVECs model was used to assess the effects of BAI through CCK8 assays, cell permeability assays, and RT-qPCR.
Results:
RNA-seq analysis revealed a set of differentially expressed genes (DEGs) shared between the Control group vs LPS group and LPS vs Baicalein group, including vascular cell adhesion molecule 1 (VCAM1), phosphoinositide-specific phospholipase C X-domain containing 1 (PLCXD1), and MIR3142 host gene (MIR3142HG), a long non-coding RNA. GO, KEGG, and Reactome enrichment analyses indicated that the DEGs were primarily enriched in TNF signaling, NF-κB signaling, and immune regulation pathways. Molecular docking and molecular dynamics simulation analyses revealed that BAI exhibits a strong binding affinity for key targets VCAM1 and PLCXD1. ROC analysis revealed that these core genes, VCAM1 and PLCXD1, exhibited significant diagnostic potential for sepsis. The cell experimental results demonstrated that BAI significantly alleviated the expression levels of inflammatory markers (such as IL-6 and IL-1β) and reduced endothelial cell permeability induced by LPS in HUVECs.
Conclusion:
BAI may alleviate LPS-induced endothelial cell injury by modulating the inflammatory response and immune microenvironment through the regulation of MIR3142HG, VCAM1, and PLCXD1 targets. This study provides new molecular targets and theoretical insights for sepsis therapy.
