Abstract

To investigate the pathological mechanism underlying the injury caused by ischemia/reperfusion and reperfusion and explore the role of ginsenoside Rg2 on ischemia/reperfusion injury to spinal cord, 24 male Sprague Dawley rats underwent a surgical procedure in this study. The rats were divided into 3 groups, group 1- sham operated group (n=8), group 2- surgical ischemia/reperfusion (n=8) and group 3- surgical ischemia/reperfusion+ginsenoside Rg2 (n=8). Oxidative stress, apoptosis and pathological indices were observed if any. Thirty minutes of ischemia, reduced the lumbar spinal cord blood flow by 77.48 % of the baseline and as the reperfusion was initiated, local blood flow increased rapidly and exceed the baseline level, and continued to below the levels of baseline later. However, it returns to baseline levels local blood perfusion after reperfusion 1 h. Last for 3 h then it drops to 207.13 %±38.25 RU, but the value of blood flow not recovery. In addition, the level of oxidative stress increased in a time-dependent manner after ischemia/reperfusion. Ginsenoside Rg2 could significantly reduce the ischemia/reperfusion-induced oxidative stress and apoptotic injury to the spinal cord in the rat. These results demonstrated that pathological mechanism changes during ischemia/reperfusion injury and with reperfusion time correlation and compliance. This study also confirmed that ginsenoside Rg2 could inhibit ischemia/reperfusion-induced oxidative stress and apoptosis in the rat spinal cord, thus providing a new insight for the treatment for ischemia/reperfusion injury of the spinal cord in future.