Resveratrol protects against vinorelbine-induced vascular endothelial cell injury

Abstract

Vinorebine (VNR), a second-generation vinca alkaloid antitumor drug, caused serious local venous toxicities, such as venous irritation, phlebitis and necrotizing vasculitis. This study investigated whether resveratrol (RES), a naturally occurring polyphenol compound, could reduce the vascular injury induced by VNR. Human vascular endothelial cell line ECV-304 cells were exposed to VNR for 10 min and then cells were cultured with serum-free medium with or without RES for 24 h. MTT (3-[4, 5-dimethyl-2-thiazolyl]-2, 5-diphe-nyl-2-tetrazolium bromide) assay was used to detect the cell viability. Reactive oxygen species (ROS) was measured with 2′, 7′-dichlorofluorescein diacetate (DCFH-DA). The activity of superoxide dismutase (SOD) was assessed by SOD detection kit. VNR decreased the viability of ECV-304 cells in a dose-dependent manner. Moreover, VNR caused cell apoptosis, the generation of intracellular ROS and the reduction of intracellular SOD. Interestingly, pretreatment with RES for 2 h increased the cell viability in a dose-dependent manner. Cell apoptosis, the intracellular ROS generation and the reduction of intracellular SOD induced by VNR were also attenuated when cells were pretreated with RES for 2 h. These results demonstrated that RES would protect against vascular endothelial cell injury induced by VNR. So the use of RES together with VNR may be a possible therapeutic approach to avoid the vascular injury induced by VNR.

• ECV-304
• endothelial injury
• resveratrol
• ROS
• vinorelbine