Increased on oxidative brain injury in the diabetic rats following sepsis

Synapse ◽  
2014 ◽  
Vol 68 (9) ◽  
pp. 410-418 ◽  
Author(s):  
Andriele Vieira ◽  
Monique Michels ◽  
Drielly Florentino ◽  
André Antunes Lauriano ◽  
Lucineia Gainski Danielski ◽  
...  
Keyword(s):  
Brain Injury ◽  
Diabetic Rats ◽  
Oxidative Brain Injury

scholarly journals Influence of exercise training on ischemic brain injury in type 1 diabetic rats

2012 ◽  
Vol 113 (7) ◽  
pp. 1121-1127 ◽  
Author(s):  
Denise M. Arrick ◽  
Hong Sun ◽  
William G. Mayhan
Keyword(s):  
Brain Injury ◽  
Exercise Training ◽  
Vascular Function ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Cerebrovascular Function ◽  
Pial Arterioles

While exercise training (ExT) appears to influence cerebrovascular function during type 1 diabetes (T1D), it is not clear whether this beneficial effect extends to protecting the brain from ischemia-induced brain injury. Thus our goal was to examine whether modest ExT could influence transient focal ischemia-induced brain injury along with nitric oxide synthase (NOS)-dependent dilation of cerebral (pial) arterioles during T1D. Sprague-Dawley rats were divided into four groups: nondiabetic sedentary, nondiabetic ExT, diabetic (streptozotocin; 50 mg/kg ip) sedentary, and diabetic ExT. In the first series of studies, we measured infarct volume in all groups of rats following right MCA occlusion for 2 h, followed by 24 h of reperfusion. In a second series of studies, a craniotomy was performed over the parietal cortex, and we measured responses of pial arterioles to an endothelial NOS (eNOS)-dependent, a neuronal NOS (nNOS)-dependent, and a NOS-independent agonist in all groups of rats. We found that sedentary diabetic rats had significantly larger total, cortical, and subcortical infarct volumes following ischemia-reperfusion than sedentary nondiabetic, nondiabetic ExT, and diabetic ExT rats. Infarct volumes were similar in sedentary nondiabetic, ExT nondiabetic, and ExT diabetic rats. In contrast, ExT did not alter infarct size in nondiabetic compared with sedentary nondiabetic rats. In addition, ExT diabetic rats had impaired eNOS- and nNOS-dependent, but not NOS-independent, vasodilation that was restored by ExT. Thus ExT of T1D rats lessened ischemic brain injury following middle cerebral artery occlusion and restored impaired eNOS- and nNOS-dependent vascular function. Since the incidence of ischemic stroke is increased during T1D, we suggest that our finding are significant in that modest ExT may be a viable preventative therapeutic approach to lessen ischemia-induced brain injury that may occur in T1D subjects.

scholarly journals Alcesefoliside protects against oxidative brain injury in rats

2019 ◽  
Vol 29 (2) ◽  
pp. 221-227
Author(s):  
Rumyana Simeonova ◽  
Vessela Vitcheva ◽  
Magdalena Kondeva-Burdina ◽  
Georgi Popov ◽  
Aleksandar Shkondrov ◽  
...  
Keyword(s):  
Brain Injury ◽  
Oxidative Brain Injury

scholarly journals Correction to: Casein micelles from bovine Milk exerts Neuroprotection by stalling metabolic complications linked to oxidative brain injury

2020 ◽  
Vol 35 (8) ◽  
pp. 1429-1429
Author(s):  
Ochuko L. Erukainure ◽  
Veronica F. Salau ◽  
Opeyemi O. Alabi ◽  
Osaretin A. T. Ebuehi ◽  
Neil A. Koorbanally ◽  
...  
Keyword(s):  
Brain Injury ◽  
Bovine Milk ◽  
Casein Micelles ◽  
Metabolic Complications ◽  
Oxidative Brain Injury

scholarly journals Oxymatrine Ameliorates Memory Impairment in Diabetic Rats by Regulating Oxidative Stress and Apoptosis: Involvement of NOX2/NOX4

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yongpan Huang ◽  
Xinliang Li ◽  
Xi Zhang ◽  
Jiayu Tang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Brain Injury ◽  
Western Blotting ◽  
Caspase 3 ◽  
Memory Function ◽  
Diabetic Rats ◽  
Oxygen Species ◽  
Expression Levels

Oxymatrine (OMT) is the major quinolizidine alkaloid extracted from the root of Sophora flavescens Ait and has been shown to exhibit a diverse range of pharmacological properties. The aim of the present study was to investigate the role of OMT in diabetic brain injury in vivo and in vitro. Diabetic rats were induced by intraperitoneal injection of a single dose of 65 mg/kg streptozotocin (STZ) and fed a high-fat and high-cholesterol diet. Memory function was assessed using a Morris water maze test. A SH-SY5Y cell injury model was induced by incubation with glucose (30 mM/l) to simulate damage in vitro. The serum fasting blood glucose, insulin, serum S100B, malondialdehyde (MDA), and superoxide dismutase (SOD) levels were analyzed using commercial kits. Morphological changes were observed using Nissl staining and electron microscopy. Cell apoptosis was assessed using Hoechst staining and TUNEL staining. NADPH oxidase (NOX) and caspase-3 activities were determined. The effects of NOX2 and NOX4 knockdown were assessed using small interfering RNA. The expression levels of NOX1, NOX2, and NOX4 were detected using reverse transcription-quantitative PCR and western blotting, and the levels of caspase-3 were detected using western blotting. The diabetic rats exhibited significantly increased plasma glucose, insulin, reactive oxygen species (ROS), S-100B, and MDA levels and decreased SOD levels. Memory function was determined by assessing the percentage of time spent in the target quadrant, the number of times the platform was crossed, escape latency, and mean path length and was found to be significantly reduced in the diabetic rats. Hyperglycemia resulted in notable brain injury, including histological changes and apoptosis in the cortex and hippocampus. The expression levels of NOX2 and NOX4 were significantly upregulated at the protein and mRNA levels, and NOX1 expression was not altered in the diabetic rats. NOX and caspase-3 activities were increased, and caspase-3 expression was upregulated in the brain tissue of diabetic rats. OMT treatment dose-dependently reversed behavioral, biochemical, and molecular changes in the diabetic rats. In vitro, high glucose resulted in increases in reactive oxygen species (ROS), MDA levels, apoptosis, and the expressions of NOX2, NOX4, and caspase-3. siRNA-mediated knockdown of NOX2 and NOX4 decreased NOX2 and NOX4 expression levels, respectively, and reduced ROS levels and apoptosis. The results of the present study suggest that OMT alleviates diabetes-associated cognitive decline, oxidative stress, and apoptosis via NOX2 and NOX4 inhibition.

Casein micelles from bovine Milk exerts Neuroprotection by stalling metabolic complications linked to oxidative brain injury

2020 ◽  
Vol 35 (8) ◽  
pp. 1417-1428
Author(s):  
Ochuko L. Erukainure ◽  
Veronica F. Salau ◽  
Opeyemi O. Alabi ◽  
Osaretin A. T. Ebuehi ◽  
Neil A. Koorbanally ◽  
...  
Keyword(s):  
Brain Injury ◽  
Bovine Milk ◽  
Casein Micelles ◽  
Metabolic Complications ◽  
Oxidative Brain Injury

Oxidative brain injury from extravasated erythrocytes after intracerebral hemorrhage

2002 ◽  
Vol 953 (1-2) ◽  
pp. 45-52 ◽  
Author(s):  
Jimin Wu ◽  
Ya Hua ◽  
Richard F Keep ◽  
Timothy Schallert ◽  
Julian T Hoff ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Oxidative Brain Injury
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