Baicalein protects against endothelial cell injury by inhibiting the TLR4/NF‑κB signaling pathway

The involvement of vascular endothelial injury with the pathophysiological process of heart failure has been identified. Baicalein (BAI), a flavonoid extracted from the root of Scutellaria baicalensis, is reported to exert antibacterial, antiviral, antithrombotic and antioxidant effects. The aim of the present study was to investigate the effects of BAI on lipopolysaccharide (LPS)‑induced vascular endothelial injury. Human umbilical vein endothelial cells (HUVECs) were stimulated by LPS (10 µM) in the presence or absence of BAI. The expressions of the inflammatory cytokines interleukin (IL)‑lβ, IL‑6, tumor necrosis factor‑α (TNF‑α) and monocyte chemoattractant protein‑1 (MCP‑1) were analyzed by reverse transcription‑quantitative polymerase chain reaction, western blotting and enzyme‑linked immunosorbent assay. Cell apoptosis was assessed by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The results showed that BAI significantly inhibited the LPS‑induced inflammatory response and apoptosis in HUVECs. BAI suppressed the LPS‑induced upregulation of IL‑1β, IL‑6, TNF‑α and MCP‑1. Furthermore, BAI decreased the expression of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and cleaved caspase‑3; however, it increased the protein level of Bcl‑2. The inhibitory effect of BAI may occur through the suppression of the Toll‑like receptor 4 (TLR4)/phosphorylated (p)‑transforming growth factor β‑activated kinase 1/tumor necrosis factor receptor‑associated family member associated nuclear factor (NF)‑κB activator‑binding kinase 1 (p‑TBK1)/NF‑κB signaling pathway. An increase in the level of p‑TBK1 by MRT67307 abolished the effect of BAI on p‑p65. In conclusion, the results of the present research suggested that BAI ameliorated endothelial cell injury associated with TLR4/NF‑κB signaling, and highlighted the potential clinical use of BAI in blocking endothelial dysfunction and preventing heart failure.