Abstract

Ischemia-reperfusion injury is one of the most important components of the pathogenesis of spinal cord dysfunction. The aim of this experimental study was to investigate the beneficial effects of Ginsenoside Rg1 (GRg1) on spinal cord ischemia-reperfusion injury and its associated mechanism. Male Sprague-Dawley (SD) rats were divided into the following ten groups: a sham group, an ischemia group, four reperfusion groups and four GRg1 groups. Spinal cord ischemia-reperfusion injury was induced by balloon occlusion of the aorta for 10 minutes, followed by immediate reperfusion. In the GRg1 treatment groups, intraperitoneal injection of GRg1 was performed 30 minutes before the induction of ischemia and immediately after the completion of ischemia. The animals were then sacrificed at designated time points, namely, 6, 12, 24 or 48 h after reperfusion had started. Histopathology (H&E staining) and immunohistochemistry (Survivin, Bcl-2, AIF and TUNEL) were performed in all the groups. Spinal cord ischemia-reperfusion produced prominent tissue damage characterized by edema and neuronal injury in the affected regions. Rats in the GRg1 treatment groups showed significantly better morphological results than those in the corresponding reperfusion groups. The numbers of survivin- and Bcl-2-positive cells in the GRg1 groups were more than that in the reperfusion groups (P < 0.05), whereas the numbers of AIF- and TUNEL-positive cells were less (P < 0.05). The data obtained in this study demonstrates a considerable neuroprotective effect of GRg1 during spinal cord ischemia-reperfusion in rats. One of the underlying mechanisms is that GRg1 reduces cell apoptosis.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.