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International Journal of Clinical and Experimental Neurology

ISSN (Print): 2379-7789

ISSN (Online): 2379-7797

Editor-in-Chief: Zhiyou Cai, MD




Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress

1Zoology Department, Faculty of Science

2Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta 31527, Egypt

International Journal of Clinical and Experimental Neurology. 2015, 3(1), 21-25
doi: 10.12691/ijcen-3-1-4
Copyright © 2015 Science and Education Publishing

Cite this paper:
Afaf El Atrash, Lamees Dawood, Ehab Tousson, Amira Salama. Neuroprotective Role of Vitamin B3 in Experimentally Induced Oxidative Stress. International Journal of Clinical and Experimental Neurology. 2015; 3(1):21-25. doi: 10.12691/ijcen-3-1-4.

Correspondence to: Ehab  Tousson, Zoology Department, Faculty of Science. Email:


Paraquat is a widely used herbicide. The main mechanism underlying PQ toxicity is oxidative stress. Niacin (nicotinic acid) a precursor for NAD+ It has also been reported to possess oxygen radical scavenging activity. The enzyme PARP-1 is activated by DNA strand breaks, using NAD+ as a substrate. Thus, the present study aimed to assess the magnitude of oxidative DNA damage and the role of PARP and the advantages of modulating its activity by niacin supplementation in experimentally induced oxidative stress by PQ. 50 male albino rats were equally divided into five groups; the first and second groups were the control and PQ treated groups respectively while the 3rd group was nicotinic acid treated group; the 4th and 5th groups were co- and post treated PQ treated rats with nicotinic acid respectively. Serum 8-hydroxy-2'-deoxyguanosine and brain MDA levels in PQ treated group showed a significant increase when compared with control group, while levels of PARP activity and TAC in PQ treated group showed a significant decrease when compared with control group. A significant increase of PARP activity & TAC and a significant decrease in serum 8-hydroxy-2'-deoxyguanosine&MDA after nicotinic acid injection when compared with control group was observed. Post-treatment with nicotinic acid improved the biochemical and histopathological alterations in brain treated with nicotinic acid, while co-treatment with nicotinic acid protected against ROS production.



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Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury

1Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan

2Research and Education Program for Life Science, The University of Fukui, Fukui, Japan

3Department of Orthopedic Surgery, Suzuki Orthopaedic Clinics, Toki, Gifu, Japan

4Department of Orthopedic Surgery, Yamada Orthopaedic Clinics, Hamamatsu, Shizuoka, Japan

5Victor Horsley Department of Neurosurgery, The National Hospital for Neurology and Neurosurgery, Queen Square, London, UK

International Journal of Clinical and Experimental Neurology. 2015, 3(2), 26-31
doi: 10.12691/ijcen-3-2-1
Copyright © 2015 Science and Education Publishing

Cite this paper:
Shigeru Kobayashi, Yoshihiko Suzuki, Syuichi Yamada, Naji Al-Khudairi, Adam Meir. Cyclooxygenase Expression in Canines Following Peripheral Nerve Injury. International Journal of Clinical and Experimental Neurology. 2015; 3(2):26-31. doi: 10.12691/ijcen-3-2-1.

Correspondence to: Shigeru  Kobayashi, Department of Orthopedics and Rehabilitation Medicine, Faculty of Medical Sciences, The University of Fukui, Fukui, Japan. Email:


In order to investigate the mechanism of neurogenic pain, this study used a median nerve compression model in dogs. The nerve was compressed with a clip for three weeks. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against cyclooxygenase (COX)-1 and 2 were used to examine the localization and changes of these mediators caused by nerve compression. In control animals, resident T cells were detected, but there were no macrophages. COX-2 was positive in the Schwann cells and vascular endothelial cells, while COX-1 was detected in the vascular endothelial cells. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for COX-2. COX-2 may be deeply involved in neuritis arising from mechanical compression, and this mediator seems to be important in the manifestation of neurogenic pain.



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Behavioral and Neurochemical Characteristics of Two Months Old WAG/Rij Rats with Genetic Absence Epilepsy

1Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia

2State Zakusov Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow, Russia

International Journal of Clinical and Experimental Neurology. 2015, 3(2), 32-44
doi: 10.12691/ijcen-3-2-2
Copyright © 2015 Science and Education Publishing

Cite this paper:
E. A. Fedosova, K. Yu. Sarkisova, V. S. Kudrin, V. B. Narkevich, A. S. Bazyan. Behavioral and Neurochemical Characteristics of Two Months Old WAG/Rij Rats with Genetic Absence Epilepsy. International Journal of Clinical and Experimental Neurology. 2015; 3(2):32-44. doi: 10.12691/ijcen-3-2-2.

Correspondence to: A.  S. Bazyan, Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow, Russia. Email:


WAG/Rij rats are genetic animal model of absence epilepsy with comorbidity of depression. The first spike-wave discharges (SWDs) in WAG/Rij rats begin to appear at the age of 2-3 months and are fully manifested by 5-6 months. Occurrence of SWDs in the EEG is the main index of absence epilepsy. Previously it has been shown that the extensive absence epilepsy in 5-6 months old WAG/Rij rats is accompanied by decrease of dopamine and its metabolites concentrations in the meso-cortico-limbic and nigro-striatal dopaminergic brain systems, resulting in the expression of depression-like behavioral symptoms, and impairments of the learning and memory processes. In 36 days old WAG/Rij rats, SWDs are not manifested, deficiency of the mesolimbic dopamine is not revealed, and symptoms of depression-like behavior are not expressed. In this study, behavior in the open field, light-dark choice, forced swimming tests, monoamines and their metabolites concentrations in 5 brain structures (prefrontal cortex, nucleus accumbens, hypothalamus, striatum, hippocampus) were investigated in two months old WAG/Rij rats in comparison with age-matched Wistar rats. Reduced concentration of the dopamine and its metabolites, and increased concentration of the serotonin was found in WAG/Rij rats compared with Wistar rats only in the prefrontal cortex, indicating that the prefrontal cortex is the brain structure where neurochemical abnormalities appear first. No substantial changes in the monoamine and their metabolites concentrations have been revealed in other brain structures. Two months old WAG/Rij rats didn’t exhibit depression-like behavior in the forced swimming test, and learning/memory deficits in the passive avoidance test, but they showed behavioral changes, indicating increase anxiety/stress-reactivity, and alterations in learning/memory in the active avoidance test. Results suggest that two month-old WAG/Rij rats are at the stage of so called “pre-pathology” (increased anxiety and stress reactivity) preceding the development of depression-like behavior and substantial cognitive impairments which are co-morbid to fully expressed absence epilepsy in 5-6 months old rats of this strain.



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