Vitamin E protects against lipid peroxidation due to cold-SO2 coexposure in mouse lung.

Exposure to sulfur dioxide (SO2) and cold increases especially in the winter. SO2 or cold exposure destroys the oxidant/antioxidant balance and increases lipid peroxidation. However, the effect of coexistence of both factors has not been studied yet. Therefore, we investigated the effect of SO2 and/or repeated short-term cold exposure on the oxidant-antioxidant status and the possible protective role of vitamin E in the cardiopulmonary tissues of mice. Swiss albino mice of both sexes were assigned to eight groups. Four groups were kept at room temperature, injected either with saline or vitamin E (100 mg/kg) in the presence or absence of SO2 exposure (10 ppm, 1 h/day, 30 days). The remaining four groups received the same protocol but were exposed to cold (4 +/- 1 degrees C, 1 h/days, 30 days) instead of room temperature. On day 30, the lung and heart tissues were removed for biochemical analysis. SO2 and cold coexposure increased lactate level in the lung, and elevated thiobarbituric acid-reactive substance (TBARS) and reduced glutathione levels in both tissues, while vitamin E treatment reversed TBARS increment predominantly in the lung. In conclusion, cold and SO2 coexposure exerts more deleterious effects in the cardiopulmonary tissues, while vitamin E treatment seems to be protective, particularly in the lung

Topiramate as a neuroprotective agent in a rat model of spinal cord injury

Topiramate (TPM) is a widely used antiepileptic and antimigraine agent which has been shown to exert neuroprotective effects in various experimental traumatic brain injury and stroke models. However, its utility in spinal cord injury has not been studied extensively. Thus, we evaluated effects of TPM on secondary cellular injury mechanisms in an experimental rat model of traumatic spinal cord injury (SCI). After rat models of thoracic contusive SCI were established by free weight-drop method, TPM (40 mg/kg) was given at 12-hour intervals for four times orally. Post TPM treatment, malondialdehyde and protein carbonyl levels were significantly reduced and reduced glutathione levels were increased, while immunoreactivity for endothelial nitric oxide synthase, inducible nitric oxide synthase, and apoptotic peptidase activating factor 1 was diminished in SCI rats. In addition, TPM treatment improved the functional recovery of SCI rats. This study suggests that administration of TPM exerts neuroprotective effects on SCI

Effects of the Glutamine on the Neuronal Cell Death in rat Ischemia-reperfusion Model

ATILLA, PERGIN/0000-0001-5132-0002WOS: 000347120800005Background: The aim of this study was to explore the effects of glutamine in brain ischemia/reperfusion model in rat. Methods: Right common carotid arteries of 24 Wistar albino rats were clamped for a duration of 30 minutes. Two hours later, except CONTROL group, glutamine was infused into left femoral vein of rats in GLIV group; and glutamine and normal saline was administered into cisterna magna of rats in GLIS and SFIS groups, respectively. After 7 days, all animals were decapitated and each brain was divided into two hemispheres for histopathological and biochemical evaluation. The right hemisphere was called "Hypoxia/Reperfusion side (HRS)" and the left hemisphere was called " Toxicity side (TS)". Results: In TS and HRS, degenerated neuron counts of GLIV groups were significantly higher than other groups' values. Degenerated neuron count values of TS were significantly lower than HRS values for GLIS, and SFIS groups, but the results of GLIV group in TS did not different from the GLIV group in HRS. LPO levels of TS and HRS of the groups was not statistically significant. Conclusion: This study results showed that glutamine had no beneficial effect to the hypoxia/reperfusion injury in rat model

Neuroprotective effects of racemic ketamine and (S)-ketamine on spinal cord injury in rat

WOS: 000305422000026PubMed: 22436574Background: The aim of this study was to investigate and to compare the potential neuroprotective effects of racemic ketamine, (S)-ketamine and methylprednisolone after an experimental spinal cord injury model in rats. Methods: Fifty-nine Wistar albino rats were divided into three main groups as acute stage (A), subacute stage (SA) and sham groups and then acute and subacute stage groups were divided into four groups regarding the used drug as control (CONT), racemic ketamine (RK), (S)-ketamine (SK) and methylprednisolone (MP) groups. A dorsal laminectomy was performed; and spinal cord injury was induced by using a temporary aneurysm clip. Four hours later from the clip compression, except those of the sham and control groups, the drugs (60 mg/kg racemic ketamine, 60 mg/kg (S)-ketamine or 30 mg/kg methylprednisolone) were administered intraperitoneally. At 72th h and 7th days of the study, the spinal cords of rats were removed from T8 level to the conus medullaris level. The specimens were and evaluated histopathologically, tissue lipid peroxidation (LPO) and myeloperoxidation (MPO) levels were measured and biochemically. Results: The histopathological results were similar both in the acute and in the subacute stage groups. There was a statistically significant difference among all groups regarding the tissue LPO levels (p < 0.001). There was a statistically significant difference between the CONT-A group and the MP-A, RK-A and SK-A groups (p = 0.004, p < 0.001 and p = 0.007, respectively) in acute stage and between the CONT-SA group and SK-SA group (p = 0.002) in subacute stage. There was a statistically significant difference among all groups regarding the tissue MPO levels (p = 0.001). The median MPO levels were similar among acute stage groups (p = 0.057), but there was a statistical difference among subacute stage groups (p = 0.046). Conclusion: (S)-ketamine is more effective than methylprednisolone and racemic ketamine to reduce the LPO levels in subacute stage of spinal cord injury in rats. And, it is as effective as methylprednisolone in preventing secondary spinal cord injury histopathologically. (c) 2012 Elsevier Ltd. All rights reserved

Neuroprotective Effect Of Magnesium Sulfate And Dexamethasone On Intrauterine Ischemia In The Fetal Rat Brain: Ultrastructural Evaluation

AIM: The aim of this study was to investigate the neuroprotective effect of magnesium sulfate and dexamethasone on oxidative damage in intrauterine ischemia. MATERIAL and METHODS: In this study, 19-day pregnant rats were divided into five groups. Fetal brain ischemia was achieved in the ischemia/reperfusion (I/R) group by bilaterally closing the utero-ovarian artery with aneurysm clips for 30 min and subsequently removing the aneurysm clips for 60 min for reperfusion. Mg (600 mg/kg) and dexamethasone (0.25 mg/kg) were administered 20 min before the I/R insult. The lipid peroxidation in the brain tissue was determined by the concentration of thiobarbituric acid reactive substances (TBARS). The mitochondrial score was calculated after an evaluation with electron microscopy. RESULTS: Both the electron microscope and TBARS data showed a significant difference between the control and I/R groups. The Mg and dexamethasone treatment groups exhibited significantly lower TBARS values compared to the IR group. Similarly, the mitochondrial scores in the Mg and dexamethasone treatment groups were significantly lower than those in the I/R group. CONCLUSION: Result showed that magnesium sulfate and dexamethasone prevent lipid peroxidation and reduce mitochondrial injury thus suggests neuroprotective effects in fetal rat brain in intrauterine ischemia-reperfusion (I/R) injury.WoSScopu

The Therapeutic Effects Of Melatonin And Nimodipine In Rats After Cerebral Cortical Injury

AIM: Secondary brain injury starts after the initial traumatic impact and marked by an increase in the intracellular calcium concentrations. This cascadeeventually results in membrane lipid peroxidation and neuronal cell death. MATERIAL and METHODS: We investigated the neuro-protective effects of nimodipine and melatonin in 38 rats after 6 hours of head trauma using the cortical impact injury model of Marmarou. RESULTS: Brain water in the melatonin-given group decreased significantly comparing to that of control group the brain water in the nimodipine given group increased significantly comparing to that of trauma group. Histopathologically, brain edema was significantly low in melatonin-administered group comparing to that of control group while there were no changes in brain edema in the nimodipine given group and in the group that both nimodipine and melatonin were administered in combination. MDA levels in the brain tissues were significantly lower in the melatonin and nimodipine groups comparing to those of trauma and control group however this difference was by far significant in melatonin group comparing to nimodipine group. CONCLUSION: Melatonin appears to have neuro-protective effects on the secondary brain damage while nimodipine and nimodipine plus melatonin combination did not show such neuro-protective effects on the secondary brain injury.WoSScopu

Evaluation of the neurotoxicity of DMSO infused into the carotid artery of rat

WOS: 000300640000013PubMed: 21907339Introduction: Despite the explanations put forth in many studies regarding histopathological evidence of the inflammatory stage related with the infusion of dimethyl sulfoxide (DMSO) in the vessel wall and its lumen, there has been no research to evaluate its neural toxicity when it is infused via the intracarotid route. This study was designed to evaluate the possible neurotoxic effects of DMSO on the closer and distant brain tissue and carotid artery when it was slowly infused into the internal carotid arteries of the rats. Methods: The right common carotid artery bifurcation was exposed through a midline neck incision, and then except those of the control group animals (n = 5), the experimental material (normal saline, n = 5 or anhydrous DMSO, n = 10) was infused into the internal carotid artery of the Wistar albino rats. After the experimental materials were administered intra-arterially, brain tissues were harvested for histopathological and biochemical studies at 72 h for investigation of the acute stage changes and on 10th day for investigation of the chronic stage changes. Internal carotid arteries of both sides were also removed for histopathological evaluation. During sacrification of the rats, whole body blood of them are collected for biochemical evaluation. Results: There was no statistically significant difference between the groups regarding comparison of the mean values of the hippocampal neuronal cell counts and the carotid artery diameters in both acute and chronic stages. Also, mean values of the lipid peroxidation levels of harvested brain tissues and serums of the collected bloods were similar in control, saline and DMSO groups. Conclusion: This experimental study suggested that DMSO has no toxic effect on the neural and arterial tissues of rats when it is slowly infused into the carotid artery. (C) 2011 Elsevier Ltd. All rights reserved

Effects of low-dose methotrexate in spinal cord injury in rats

WOS: 000322097200002PubMed: 23884668BACKGROUND This study was designed to evaluate the possible protective effects of low-dose methotrexate in the spinal cord injury (SCI) in rats. METHODS Thirty-seven Wistar albino rats were used in the present study. Except for the animals of the Sham group, all animals were divided into two main groups, which were used in acute and subacute stage investigations. Then, thoracal laminectomy was performed, and except for the Sham group, SCI was induced using a temporary aneurysm clip. After clip compression, the experimental material (methotrexate or methylprednisolone) was administered intraperitoneally, except in the Sham and Control groups. Then, the spinal cords were removed to evaluate the SCI histopathologically and biochemically at the scheduled date. RESULTS Neither experimental material was shown to reduce the histopathological grade in either stage of SCI. Low-dose methotrexate was shown to decrease lipid peroxidation levels only in the subacute stage of SCI. However, methylprednisolone and low-dose methotrexate could not decrease or block myeloperoxidase enzyme activation in either stage of SCI. CONCLUSION Low-dose methotrexate was effective in reducing the lipid peroxidation levels in the subacute stage of SCI, although histopathological evaluation results and myeloperoxidase levels of all groups did not support this finding at either stage

Effects Of Intracisternal And Intravenous Dexmedetomidine On Ischemia-Induced Brain Injury In Rat: A Comparative Study

AIM: To compare the effect of dexmedetomidine administered by intracisternal route with by intravenous route on brain tissue of rat after incomplete cerebral ischemia. MATERIAL and METHODS: Cerebral ischemia was produced by the combination of right common carotid artery occlusion and hemorrhagic hypotension during 30 minutes. Thirty minutes before the ischemia, 0.1 ml 0.9% NaCl (Group SIC, n=6) or 9 mu g/kg dexmedetomidine (Group DIC, n=6) was administered into the cisterna magna. For the intravenous groups, 9 mu g/kg dexmedetomidine (Group DIV, n=6) or 0.9% NaCl (Group CONTROL, n=6) 5 ml/kg/h was given in 2 hours. After 24 hours, the lipid peroxidation levels were measured in the brain tissue and plasma. Hippocampal formations were used for histopathological examination. RESULTS: Intravenous dexmedetomidine produced a decrease in baseline mean arterial blood pressure and plasma glucose concentrations. There was a significant difference between the DIV group and DIC, SIC, CONTROL groups regarding the brain lipid peroxidation levels (p<0.001, p<0.001, p=0.001, respectively), and regarding the picnotic neuronal cell count (p<0.001, p=0.01, p=0.009, respectively). Mean plasma lipid peroxidation levels of the DIV group was different from the DIC group (p=0.003). CONCLUSION: Systemically administered dexmedetomidine had neuroprotective effect in ischemia-induced neuronal damage, but centrally administered dexmedetomidine did not.WoSScopu