Neuroprotective effects of resveratrol against traumatic brain injury in immature rats

Childhood trauma resulting in traumatic brain injury (TBI) due to accidents and abuse is the major cause of death and dysfunction in the young. Since there are no approved specific pharmacological agents that block the progression of the secondary injury, the current management of TBI is mainly supportive. We aimed to determine the effect of resveratrol on hippocampal damage and behavioral deficits in 7-day-old rat pups subjected to contusion injury. Resveratrol was injected intraperitoneally at the doses of 100 mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining and behavioral alterations were evaluated using open field and novel object recognition tests 2 weeks after trauma. Histopathological evaluation showed that treatment with a single dose of 100 mg/kg resveratrol (i.p.) after the trauma significantly ameliorated the trauma induced hippocampal neuron loss at ipsilateral and contralateral hippocampal brain regions of rats. Additionally, treatment with resveratrol decreased anxiety and increased cortex/hippocampus dependent memory of animals subjected to blunt head trauma. These results show that acute treatment of resveratrol has a neuroprotective role against trauma induced hippocampal neuron loss and associated cognitive impairment in rats. (c) 2007 Elsevier Ireland Ltd. All rights reserved

Protective effect of melatonin against maternal deprivation-induced acute hippocampal damage in infant rats

It is known that maternal deprivation induces hippocampal damage in the developing brains. In the present study, we examined the effects of melatonin on maternal deprivation-induced hippocampal damage both during and after stress-hyporesponsive period (SHRP). Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. The results showed that a single episode of maternal deprivation for 24 It at post-SHRP induced neuronal loss in hippocampus regions of the brain in the infant rats, while it did not influence hippocampal neurons in SHRP. Melatonin prevented maternal deprivation-induced hippocampal damage in the infant rats at post-SHRP. These results suggest that melatonin is a potentially beneficial agent to improve the neurobehavioral outcomes of maternal deprivation in later developmental period. (C) 2006 Elsevier Ireland Ltd. All rights reserved

Erythropoietin attenuates neuronal injury and potentiates the expression of pCREB in anterior horn after transient spinal cord ischemia in rats

Background: Recent studies have suggested that EPO activates the CREB transcription pathway and increases BDNF expression and production, which contributes to EPO-mediated neuroprotection. We investigated whether EPO has a neuroprotective effect against ISCI in rats and examined the involvement of CREB protein phosphorylation in this process

Methamphetamine induces oligodendroglial cell death in vitro

We investigated whether the psychostimulant methamphetamine (METH) has a cytotoxic effect on oligodendrocytes and which cell-death pathways are involved in the cytotoxic process. METH caused concentration- and time-dependent cytotoxicity in rat oligodendrocyte cultures. METH induced apoptotic cell death and mRNA expression of pro-apoptotic proteins (bax and DP5), but not anti-apoptotic proteins (bcl-2 and bcl-XL). These results suggest that METH induces cytotoxicity in rat oligodendrocytes via the differential regulation of the expression of genes involved in the apoptotic process. (C) 2003 Elsevier B.V. All rights reserved

Protective effect of melatonin against head trauma-induced hippocampal damage and spatial memory deficits in immature rats

It is well known that head trauma induces the cognitive dysfunction resulted from hippocampal damage. In the present study, we aimed to demonstrate the effect of melatonin on hippocampal damage and spatial memory deficits in 7-day-old rat pups subjected to contusion injury. Melatonin was injected intraperitoneally at the doses of 5 or 20 mg/kg of body weight immediately after induction of traumatic injury. Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Spatial memory performance was assessed in the Morris water maze. Melatonin significantly attenuated trauma-induced neuronal death in hippocampal CA1, CA3 regions and dentate gyrus, and improved spatial memory deficits, which was equally effective at doses of 5-20 mg/kg. The present results suggest that melatonin is a highly promising agent for preventing the unfavorable outcomes of traumatic brain injury in young children. (c) 2005 Elsevier Ireland Ltd. All rights reserved

Histological and biochemical findings in an experimental model of intervertebral disc degeneration based on radio frequency

The aim of this study is to develop an disc degeneration animal model which can be standardized, easy performed and which gives quickly results by using radiofrequency. For disc degeneration New Zealand rabbits were used. Animals were divided into three groups. First group was control. The second group was examined histological 15 days after the experiment for the early period findings. The last group was examined histological and biochemical 30 days after the experiment. Nucleoplasty device was applied to different disc levels in different doses. For histological evaluation, chondrocyt like cells were numbered and thicknesses of the collagen fibers were measured in the nucleosus pulposus. Biochemically, collagen weight and percentage decrease in liquid content of nucleosus pulposus were measured. When the results of the study groups were compared with the controls, thickened collagen bands and increased number of chondrocyt like cells were detected in favour of the study groups 15 days after the experiment. Microscopic measurements of intervertebral disc were statistically significantly increased on the 30(th) day of the experiment compared with the 15(th) day results (p<0.05). As biochemical, statistically significantly reduced in the amount of collagen and percentage decrease in the liquid content of nucleus pulposus in study groups compared with the controls support degeneration(p<0.05). Our study group suggests that use of radiofrequency which was applied in a disc degeneration model is an effective, reliable and quick method and our model will help future molecular studies of disc degeneration

Prophylactic and Therapeutic Effects of Carnosine in Ischemia Reperfusion Injury of Liver

Objective: Ischemia followed by reperfusion (IR) results in hepatocyte injury and apoptosis. Current study aims to investigate the prophylactic and therapeutic effects of antioxidant carnosine in liver ischemia and reperfusion injury in rats. Material and Methods: Five groups were formed with Wistar Albino female rats: Control group, IR group, Prophylaxis group (Carnosine and IR), Therapeutic group (IR + Carnosine), Prophylaxis and therapeutic group (Carnosine + IR + Carnosine). Total hepatic ischemia for 30 minutes and reperfusion for one week were administrated. Carnosine was given with 100 mg/day for one week. Tissue samples were prepared for histopathological, immunohistochemical and ultrastructural assessment. In addition, serum ALT and AST levels were determined. Results: In IR group, neutrophilic infiltration, sinusoidal dilatation, congestion and necrotic hepatocytes in some areas were observed. Ultrastructural assessment showed mitochondrial swelling and dilatation in granular endoplasmic reticulum (GER) cisterns. In prophylaxis group, localized collagen fibrils were observed in some Disse spaces. GER cisterns were dilated in therapeutic group. All cellular structures of prophylaxis and therapeutic group were similar to control group. In IR group, TUNEL positive hepatocyte count was higher than control group. In IR group, there was strong Bax labeling in hepatocytes. However, apoptotic cell count was the smallest in prophylaxis and therapeutic group followed by therapy after prophylaxis group. In IR group, Bcl-2 immune reaction was not observed whereas there was strong expression in prophylaxis and therapeutic group. Conclusion: In IR injury of liver, administration of carnosine in both prophylaxis and therapy instead of solely therapeutic or prophylactic administration prevents the apoptosis and structural changes

Prophylactic and Therapeutic Effects of Carnosine in Ischemia Reperfusion Injury of Liver

Objective: Ischemia followed by reperfusion (IR) results in hepatocyte injury and apoptosis. Current study aims to investigate the prophylactic and therapeutic effects of antioxidant carnosine in liver ischemia and reperfusion injury in rats. Material and Methods: Five groups were formed with Wistar Albino female rats: Control group, IR group, Prophylaxis group (Carnosine and IR), Therapeutic group (IR + Carnosine), Prophylaxis and therapeutic group (Carnosine + IR + Carnosine). Total hepatic ischemia for 30 minutes and reperfusion for one week were administrated. Carnosine was given with 100 mg/day for one week. Tissue samples were prepared for histopathological, immunohistochemical and ultrastructural assessment. In addition, serum ALT and AST levels were determined. Results: In IR group, neutrophilic infiltration, sinusoidal dilatation, congestion and necrotic hepatocytes in some areas were observed. Ultrastructural assessment showed mitochondrial swelling and dilatation in granular endoplasmic reticulum (GER) cisterns. In prophylaxis group, localized collagen fibrils were observed in some Disse spaces. GER cisterns were dilated in therapeutic group. All cellular structures of prophylaxis and therapeutic group were similar to control group. In IR group, TUNEL positive hepatocyte count was higher than control group. In IR group, there was strong Bax labeling in hepatocytes. However, apoptotic cell count was the smallest in prophylaxis and therapeutic group followed by therapy after prophylaxis group. In IR group, Bcl-2 immune reaction was not observed whereas there was strong expression in prophylaxis and therapeutic group. Conclusion: In IR injury of liver, administration of carnosine in both prophylaxis and therapy instead of solely therapeutic or prophylactic administration prevents the apoptosis and structural changes

The effects of intravitreally injected bevacizumab on the retina and retina pigment epithelium: experimental in-vivo electron microscopic study in intact versus vitrectomized eyes

To analyze the retinal toxicity of bevacizumab at various doses both in vitrectomized and non-vitrectomized rabbit models. Twenty-eight rabbits were included in the study. Twenty-four rabbits were assigned to six groups, with 4 of the rabbits in the control group. The animals in Groups 1, 2 and 3 received bevacizumab at a dose of 0.3 mg, 0.5 mg and 1.5 mg/eye, respectively. The rabbits in Groups 4, 5 and 6 received intravitreal bevacizumab of 0.3 mg, 0.5 mg and 1.5mg/eye, respectively, after gas compression vitrectomy. Two weeks after the procedure, the rabbits were euthanized. Retina tissue samples were then obtained and examined with both light and electron microscopes. In Groups 1, 2 and 3 after bevacizumab injection, toxic degeneration in the photoreceptor and retinal pigment epithelium cells was observed via electron microscopic examination. The findings in Groups 4 and 5 were normal as compared to the control group. In Group 6, toxicity in the bipolar neurons and photoreceptor cells was noticed. Increased toxicity and retinal penetration were noticed in all administered doses of bevacizumab in the presence of vitreous. In addition, ocular toxicity occurred through the injection of the highest dose of bevacizumab after vitrectomy. It is possible that the bevacizumab dose and the, vitreous are as important as the drug half-life in the vitreous