[Effect of Tacrolimus on pyramidal cells of cerebral cortex in experimental brain ischemia model in Wistar rat]

Cerebral ischemia is known as a main cause of morbidity and mortality in the world and there was no effective treatment yet. Global cerebral ischemia causes loss of pyramidal cells of brain cortex following global ischemic/reperfusion. Recently, using immunophilin ligands has been considered as a potential and appropriate strategy for neuroprotection. Since it was observed that tacrolimus [FK506], a useful immunosuppressant used in organ transplantation, provides neuroprotection and prevents neuronal damage,the importance of immunophilins in the development of neuroprotectors has emerged. In this study, we investigated the neurotrophic effect of the immunosuppressant agent FK506 in rat after global cerebral ischemia. In this experimental study, 25 Wistar rats were assigned to control [intact], ischemia and 3 FK506 treated [1, 3, 6 mg/kg] groups. Both common carotid arteries were occluded for 20 minutes followed by reperfusion. In 3 experimental groups, tacrolimus or FK506 was given as a single dose exactly at the time of reperfusion respectively as 1, 3, 6 mg/kg by intravenous administration [IV]. The same doses repeated by intraperitoneally administration [IP] 48 hours after reperfusion. After 4 days, the rats were sacrificed and brain sections were stained by H and E and Nissl. Our findings showed that 20 min ischemia decreased the number of the cortex pyramidal cells. But there were significant differences between number of cortex pyramidal cells in ischemia and FK506 [6mg/kg] groups. Our study suggests that tacrolimus has a neurotrophic effect on pyramidal cells of brain cortex and may candidate for treatment of ischemia brain damage

[ effect of pentoxifylline on global ischemia/reperfusion induced spatial memory impairment in estrous phase of female wistar rat]

The short break in cerebral blood flow causes permanent brain injury and behavioral dysfunction. The hippocampus, specifically the CA1 pyramidal cells, is highly vulnerable to ischemic injuries. There is no effective pharmacological strategy for improving brain tissue damage induced by cerebral ischemia. Previous studies reported that pentoxifylline has a neuroprotective effect on brain trauma and it is well known that endogenous estrogen improves stroke outcome during vascular occlusion. In this study, the possible positive effects of pentoxifylline and estrogen on behavioral deficit and neuronal damage were studied in female Wistar rats in estrous phase subjected to an experimental model of transient global brain ischemia. In this experimental study, female Wistar rats [n= 56] were assigned to control, ischemia, vehicle, and pentoxifylline - treated [200 mg/kg IP] groups and all of them were in their estrous phase. Pentoxifylline was administered at 1 h before and 1 h after ischemia. Global cerebral ischemia was induced by bilateral common carotid artery occlusion, followed by reperfusion.Morris water maze and nissl staining was used for all groups. According to Morris water maze test results, cerebral ischemia could not exert any negative effect on cognitive spatial abilities after reperfusion and there were no significant differences between groups. In Nissl study, there were significant differences between number of pyramidal cells in both control and pentoxifylline - treated groups [P