Conversely, in vitro treatment with the pro-inflammatory endotoxin lipopolysaccharide, which activates endothelial TRPC6 in a Toll-like receptor type 4 (TLR4)-dependent manner, worsened aortic endothelial dysfunction in wild type mice.
The present results demonstrate that paeonol reduces LPS-induced endothelial dysfunction and apoptosis by inhibiting TLR4 and BMP4 signaling independently.
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.