The histological effects of ginkgo biloba extract (egb 761) and selenium on brain tissue in experimental ischemia-reperfusion injury

The Histological Effects of Ginkgo Biloba Extract (EGb 761) and Selenium on Brain Tissue in Experimental Ischemia-Reperfusion Injury Dr. Seda Özbal Histology and Embryology Department, Faculty of Medicine, Dokuz Eylül University, nciraltı, zmir, Turkey AM The brain tissue exhibits high sensitivity to ischemia-reperfusion injury and therefore, brain ischemia and consecutive reperfusion result in neural damage and apoptosis. We aimed to investigate the therapeutic effects of ginkgo biloba extract (G) and selenium (S) on the prefrontal cortex and hippocampus structural, immunohistochemically and biochemically in our experimental model. MATERIAL AND METHOD 5 study groups were formed with 4 rats in the Sham group and 14 rats in each of the remaining four groups. I. Sham, II. Ischemia-reperfusion (IR), III. IR+G, IV. IR+S, V. IR+G+S. Unilateral common carotid artery occlusion was applied 45 minutes except sham. The G, S and G+S treatments were carried out for 14 days after ischemiareperfusion, intraperitoneally. Ginkgo biloba extract was administered at a dose of 50 mg/day and selenium was administered at a dose of 0.625 mg/kg/day. The sections obtained were stained with Crezyl-violet for light microscopical examination. Apostain and Caspase-3 immune staining were used to detect apoptosis. TNF-alfa and IL- 1beta were measured in serum and TNF-alfa, IL?1beta and NGF levels were measured in prefrontal cortex and hippocampus tissue homogenates. RESULTS Marked contraction in the neurons, irregularities in cell and nucleus borders, chromatin condensation in nucleus, an increase in the density of the cytoplasm of neurons and perineural and pericapillary edema were observed in the IR group whereas these findings were highly decreased in the treatment groups. The cell count revealed that there was a decrease in the number of cells in the IR group while such a decrease was not observed in the treatment groups. While the apoptotic cells were markly stained in apostain and caspase-3 sections, these cells was not observed in treatment groups. The increased serum and tissue levels of TNF-alfa and IL?1beta and the decreased NGF levels were found to be consistent with the sham group. CONCLUSION As G, S and G+S treated groups evaluated in terms of histological and biochemical results, it was observed that each treatment group was significantly effective against cerebral ischemia-reperfusion injury in different levels.