The Effect of Vitamin E Succinate on Ischemia Reperfusion Injury

Abstract

Ischemia–reperfusion (I/R) injury is, in part, related to the burst of reactive oxygen species (ROS) generated after reperfusion. Vitamin E has been shown to exert its biological effects as an antioxidant, inhibiting the ROS. In this report, the effect of Vitamin E succinate (VES) on ischemia/reperfusion injury and NF-κB expression was studied in a rat skeletal muscle model during reperfusion following a 4-h ischemic period. The study group consisted of muscle flaps infused with 150 mg/kg of VES given intraperitoneally 1 h post-initiation of ischemia. Muscle viability based on nitroblue tetrazolium staining, edema, and Doppler blood flow was measured in a control and a study group. Muscle samples were analyzed by standard gel shift assay. The VES experimental group showed an increase in muscle viability compared to controls (average of 44.675% versus 31.925%, respectively, p=0.0415). Blood flow, measured by Doppler 24 h after reperfusion, was increased in the VES study group compared to controls (10.3 vs. 5.1 ml/g/s p=0.00355). Additionally, the VES group showed a trend of decreasing edema compared with the control; however, not at a level that was statistically significant (p=0.1267). The VES-treated group showed a decreased expression of NF-κB as compared to controls (p<0.05). These results show that vitamin E succinate has a protective effect in preventing I/R injury as measured by increased muscle viability and reperfusion blood flow. Vitamin E can exert its efforts as an antioxidant as well as other biological roles, including inhibition of NF-κB.