The Experts below are selected from a list of 9801 Experts worldwide ranked by ideXlab platform
Furong Wang - One of the best experts on this subject based on the ideXlab platform.
-
intranasal nerve growth factor attenuating the seizure onset via p75r caspase pathway in the Experimental Epilepsy
Brain Research Bulletin, 2017Co-Authors: Jingan Lei, Fang Feng, Yuanyuan Duan, Zhiguang Liu, Lifei Lian, Qiming Liang, Na Zhang, Furong WangAbstract:Abstract Background Nerve growth factor (NGF) shows neuroprotection while it is hard to cross the blood-brain barrier due to its large molecular weight. Our study used intranasal delivery of NGF to treat the Experimental Epilepsy. Methods The seizure was induced by injection of pentylenetetrazol (40 mg/kg) into the rat. Based on the behavior performance, the successful models were randomized into control and NGF groups, given medium or NGF intranasally, respectively. The onset and duration of seizure were recorded. The neuron loss was assessed by immunohistochemistry and TUNEL staining. The expressions of Caspase-3, p75R and TrkA were measured by western blotting. Results Intranasal NGF significantly reduced the seizure onset and shortened the seizure duration. Intranasal NGF alleviated the neuron loss in the epileptic brain. The number of TUNEL-positive cells in the NGF group was less than that in the control group ( P Conclusion Intranasal NGF protected neurons in the epileptic brain by inactivation of p75R/Caspase pathway. Intranasal NGF may be a novel therapeutic strategy for Epilepsy.
-
Intranasal nerve growth factor attenuating the seizure onset via p75R/Caspase pathway in the Experimental Epilepsy.
Brain research bulletin, 2017Co-Authors: Jing’an Lei, Fang Feng, Yuanyuan Duan, Zhiguang Liu, Lifei Lian, Qiming Liang, Na Zhang, Furong WangAbstract:Abstract Background Nerve growth factor (NGF) shows neuroprotection while it is hard to cross the blood-brain barrier due to its large molecular weight. Our study used intranasal delivery of NGF to treat the Experimental Epilepsy. Methods The seizure was induced by injection of pentylenetetrazol (40 mg/kg) into the rat. Based on the behavior performance, the successful models were randomized into control and NGF groups, given medium or NGF intranasally, respectively. The onset and duration of seizure were recorded. The neuron loss was assessed by immunohistochemistry and TUNEL staining. The expressions of Caspase-3, p75R and TrkA were measured by western blotting. Results Intranasal NGF significantly reduced the seizure onset and shortened the seizure duration. Intranasal NGF alleviated the neuron loss in the epileptic brain. The number of TUNEL-positive cells in the NGF group was less than that in the control group ( P Conclusion Intranasal NGF protected neurons in the epileptic brain by inactivation of p75R/Caspase pathway. Intranasal NGF may be a novel therapeutic strategy for Epilepsy.
Vahram Haroutunian - One of the best experts on this subject based on the ideXlab platform.
-
cns oxidative stress associated with the kainic acid rodent model of Experimental Epilepsy
Epilepsy Research, 2000Co-Authors: Martin R. Gluck, Elizabeth Jayatilleke, Spencer Shaw, James A Rowan, Vahram HaroutunianAbstract:The role of oxidative stress in seizure-induced brain injury was investigated in a kainic acid model of Experimental Epilepsy. Kainic acid (12.5 mg/kg) or saline was injected intraperitoneally into 12-week-old male Fischer 344 rats and sacrificed by decapitation at 4 and 24 h after injection. Markers of oxidative stress including protein carbonyls, thiobarbituric acid reactive material (TBARs), glutathione (GSH) and glutathione disulfide (GSSG) were measured in hippocampus, cortex, cerebellum and basal ganglia. Four hours after treatment, protein carbonyls were elevated by 103, 55, 52 and 32% in cortex, hippocampus, basal ganglia and cerebellum, respectively. TBARs were increased by 30–45% in all areas. After 24 h, elevated protein and lipid oxidative markers persisted in the hippocampus and cerebellum; by contrast, in the cortex, TBARs almost normalized to control values and protein carbonyls trended downward by one-half compared with measurements at 4 h, although this reduction relative to the 4 h timepoint did not reach statistical significance. In the basal ganglia, protein carbonyls approached control values at 24 h. GSSG levels were only increased statistically in the cortex after 4 h. GSH levels in all the regions were unchanged after treatment with kainic acid. However, in cortex, GSH levels correlated negatively with increases in protein and lipid oxidation (r=−0.69, P<0.002). In contrast, significant correlations between GSH, protein carbonyls and TBARs measured in the hippocampus or cerebellum were not observed. Our data suggests that kainic acid induced similar oxidative stress in all of the brain regions that were examined, and that GSH plays a major antioxidant role in the cerebral cortex but not the hippocampus.
-
CNS oxidative stress associated with the kainic acid rodent model of Experimental Epilepsy.
Epilepsy research, 2000Co-Authors: Martin R. Gluck, Elizabeth Jayatilleke, Spencer Shaw, A. James Rowan, Vahram HaroutunianAbstract:The role of oxidative stress in seizure-induced brain injury was investigated in a kainic acid model of Experimental Epilepsy. Kainic acid (12.5 mg/kg) or saline was injected intraperitoneally into 12-week-old male Fischer 344 rats and sacrificed by decapitation at 4 and 24 h after injection. Markers of oxidative stress including protein carbonyls, thiobarbituric acid reactive material (TBARs), glutathione (GSH) and glutathione disulfide (GSSG) were measured in hippocampus, cortex, cerebellum and basal ganglia. Four hours after treatment, protein carbonyls were elevated by 103, 55, 52 and 32% in cortex, hippocampus, basal ganglia and cerebellum, respectively. TBARs were increased by 30–45% in all areas. After 24 h, elevated protein and lipid oxidative markers persisted in the hippocampus and cerebellum; by contrast, in the cortex, TBARs almost normalized to control values and protein carbonyls trended downward by one-half compared with measurements at 4 h, although this reduction relative to the 4 h timepoint did not reach statistical significance. In the basal ganglia, protein carbonyls approached control values at 24 h. GSSG levels were only increased statistically in the cortex after 4 h. GSH levels in all the regions were unchanged after treatment with kainic acid. However, in cortex, GSH levels correlated negatively with increases in protein and lipid oxidation (r=−0.69, P
G. Rodríguez De Lores Arnaiz - One of the best experts on this subject based on the ideXlab platform.
-
Regional vulnerability to oxidative stress in a model of Experimental Epilepsy
Neurochemical Research, 1998Co-Authors: S. Lores Arnaiz, M. Travacio, S. Llesuy, G. Rodríguez De Lores ArnaizAbstract:We evaluated oxidative stress associated with a model of Experimental Epilepsy. Male Wistar rats were injected i.p. with 150 mg/kg convulsant 3-mercaptopropionic acid and decapitated in two stages: during seizures or in the post-seizure period. Spontaneous chemiluminescence, levels of thiobarbituric acid reactive substances, total antioxidant capacity and antioxidant enzyme activities were measured in cerebellum, hippocampus, cerebral cortex and striatum. In animals killed at seizure, increases of 42% and 90% were observed in spontaneous chemiluminescence of cerebellum and cerebral cortex homogenates, respectively, accompanied by a 25% increase in cerebral cortex levels of thiobarbituric acid reactive substances. In the post-seizure stage, emission completely returned to control levels in cerebral cortex and partly in cerebellum, thus showing oxidative stress reversibility in time. Hippocampus and striatum seemed less vulnerable areas to oxidative damage. A 30% decrease in glutathione peroxidase activity was only observed in cerebral cortex during seizures, while catalase and superoxide dismutase remained unchanged in all four areas during either stage. Likewise, total antioxidant capacity was unaffected in any of the studied areas. It is suggested that oxidative stress in this model of Epilepsy arises from an increase in oxidant species rather than from depletion of antioxidant defences.
Miguel Condés-lara - One of the best experts on this subject based on the ideXlab platform.
-
NADPH-diaphorase-stained neurons after Experimental Epilepsy in rats.
Nitric oxide : biology and chemistry, 1997Co-Authors: Esther Talavera, G. Martınez-lorenzana, Gabriel Corkidi, Martha León-olea, Miguel Condés-laraAbstract:Abstract The aim of this study was to determine the neuronal participation of nitric oxide (NO) in Experimental Epilepsy. To reach this objective, we established the amount of cells presenting nitric oxide synthase (NOS) and the amygdaline concentrations in the l -arginine–nitric oxide synthesis pathway. A group of fully epileptic rats, induced by the kindling procedure and that had reached at least 10 generalized seizures, was studied. We evaluated behavioral stages, electroencephalographic activities, and histochemical NOS-positive cells and carried out high-pressure liquid chromatography (HPLC) determinations of arginine, citrulline, and glutamic acid. Our results showed that behavioral and electrographic frequency, and duration of epileptic activities, were increased during the kindling process. Image processing system of NOS cells showed two types of intensities in cell stains in hippocampus, caudate-putamen, and amygdala. When we independently counted the two types of NOS stain cells, a selective increase in the number and density of weak-stained cells was observed, while dark-stained cells did not change in the studied structures. Additionally, arginine, citrulline, and glutamic acid concentrations in amygdala increased in kindled animals. The differential and specific increase in the stained cells expressing the nitric oxide synthase, as well as the increase in concentrations of the l -arginine–nitric oxide pathway in amygdala, suggested a relationship with the progressive augmentation in the electrophysiological hyperactivity characteristic of generalized Epilepsy.
Martin R. Gluck - One of the best experts on this subject based on the ideXlab platform.
-
cns oxidative stress associated with the kainic acid rodent model of Experimental Epilepsy
Epilepsy Research, 2000Co-Authors: Martin R. Gluck, Elizabeth Jayatilleke, Spencer Shaw, James A Rowan, Vahram HaroutunianAbstract:The role of oxidative stress in seizure-induced brain injury was investigated in a kainic acid model of Experimental Epilepsy. Kainic acid (12.5 mg/kg) or saline was injected intraperitoneally into 12-week-old male Fischer 344 rats and sacrificed by decapitation at 4 and 24 h after injection. Markers of oxidative stress including protein carbonyls, thiobarbituric acid reactive material (TBARs), glutathione (GSH) and glutathione disulfide (GSSG) were measured in hippocampus, cortex, cerebellum and basal ganglia. Four hours after treatment, protein carbonyls were elevated by 103, 55, 52 and 32% in cortex, hippocampus, basal ganglia and cerebellum, respectively. TBARs were increased by 30–45% in all areas. After 24 h, elevated protein and lipid oxidative markers persisted in the hippocampus and cerebellum; by contrast, in the cortex, TBARs almost normalized to control values and protein carbonyls trended downward by one-half compared with measurements at 4 h, although this reduction relative to the 4 h timepoint did not reach statistical significance. In the basal ganglia, protein carbonyls approached control values at 24 h. GSSG levels were only increased statistically in the cortex after 4 h. GSH levels in all the regions were unchanged after treatment with kainic acid. However, in cortex, GSH levels correlated negatively with increases in protein and lipid oxidation (r=−0.69, P<0.002). In contrast, significant correlations between GSH, protein carbonyls and TBARs measured in the hippocampus or cerebellum were not observed. Our data suggests that kainic acid induced similar oxidative stress in all of the brain regions that were examined, and that GSH plays a major antioxidant role in the cerebral cortex but not the hippocampus.
-
CNS oxidative stress associated with the kainic acid rodent model of Experimental Epilepsy.
Epilepsy research, 2000Co-Authors: Martin R. Gluck, Elizabeth Jayatilleke, Spencer Shaw, A. James Rowan, Vahram HaroutunianAbstract:The role of oxidative stress in seizure-induced brain injury was investigated in a kainic acid model of Experimental Epilepsy. Kainic acid (12.5 mg/kg) or saline was injected intraperitoneally into 12-week-old male Fischer 344 rats and sacrificed by decapitation at 4 and 24 h after injection. Markers of oxidative stress including protein carbonyls, thiobarbituric acid reactive material (TBARs), glutathione (GSH) and glutathione disulfide (GSSG) were measured in hippocampus, cortex, cerebellum and basal ganglia. Four hours after treatment, protein carbonyls were elevated by 103, 55, 52 and 32% in cortex, hippocampus, basal ganglia and cerebellum, respectively. TBARs were increased by 30–45% in all areas. After 24 h, elevated protein and lipid oxidative markers persisted in the hippocampus and cerebellum; by contrast, in the cortex, TBARs almost normalized to control values and protein carbonyls trended downward by one-half compared with measurements at 4 h, although this reduction relative to the 4 h timepoint did not reach statistical significance. In the basal ganglia, protein carbonyls approached control values at 24 h. GSSG levels were only increased statistically in the cortex after 4 h. GSH levels in all the regions were unchanged after treatment with kainic acid. However, in cortex, GSH levels correlated negatively with increases in protein and lipid oxidation (r=−0.69, P
