Fisetin inhibits high-glucose-induced vascular inflammation in vitro and in vivo.

AIM AND OBJECTIVE

Fisetin, an active compound isolated from flowering plants in the family Fabaceae, was reported to have antiviral, neuroprotective, and anti-inflammatory effects. Vascular inflammatory processes have been suggested to play key roles in the initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Thus, we determined the ability of fisetin to suppress vascular inflammatory processes induced by high glucose (HG) in primary human umbilical vein endothelial cells (HUVECs) and mice.

METHODS

The effects of fisetin on HG-induced vascular inflammation were determined by measuring vascular permeability, leukocyte adhesion and migration, cell adhesion molecule (CAM) expression levels, reactive oxygen species (ROS) formation, and nuclear factor (NF)-κB activation.

RESULTS

HG markedly increased vascular permeability, monocyte adhesion, expressions of CAMs, formation of ROS, and activation of NF-κB. Remarkably, all of the observed vascular inflammatory effects induced by HG were inhibited by pretreatment with fisetin.

CONCLUSION

Vascular inflammatory responses induced by HG are critical events underlying the development of diabetic complications; therefore, our results suggest that fisetin possesses significant therapeutic effects against diabetic complications and atherosclerosis.