A. Salama, Wafaa M. Ibrahim, E. Tousson, S. Sakr, A. Masoud, Mohamed A. Akela, Mahmoud A. Abd El-Rahman
Epigenetic modifications are defined as mechanisms that are able to modify the expression levels of selected genes without necessarily altering their DNA sequence, as histone tail modifications. These modifications are likely to contribute to the onset and progression of complex human diseases including neurodegenerative ones. Oxidative stress also is thought to be a common underlying mechanism that leads to cellular dysfunction and demise in PD. This study was aimed to assess the epigenetic fingerprint in PD experimental model through HDAC, PARP and activities oxidative stress markers. Materials and methods: The study was carried out on five rat groups, control group, Parkinsonism group, sodium butyrate group, two parkinson’s disease groups co-treated and post treated with sodium butyrate. Parkinsonism was induced by ip injection of paraquat. Laboratory measurements included serum 8-OHdG, MDA level as biomarkers of oxidative stress. HDAC and PARP activities were measured as other epigenetic mechanisms. Results: PD group, PD co-treated and post treated with sodium butyrate showed significant increase in HDAC and PARP activities. Also, there was significant increase in serum 8-OHdG level and MDA level in both serum and tissue. Conclusion and recommendations: The increments in HDAC and PARP activities are either two of the pathogenic mechanisms of the disease or it affords PD patients neuroprotection and benefits. Also, sodium butyrate is one of best antioxidant and neuroprotective agents. We recommended for further studies in HDAC and sodium butyrate as inhibitor in neurodegerative diseases, other diseases and normal state.
{"title":"Epigenetic Study of Parkinson's Disease in Experimental Animal Model","authors":"A. Salama, Wafaa M. Ibrahim, E. Tousson, S. Sakr, A. Masoud, Mohamed A. Akela, Mahmoud A. Abd El-Rahman","doi":"10.12691/IJCEN-3-1-3","DOIUrl":"https://doi.org/10.12691/IJCEN-3-1-3","url":null,"abstract":"Epigenetic modifications are defined as mechanisms that are able to modify the expression levels of selected genes without necessarily altering their DNA sequence, as histone tail modifications. These modifications are likely to contribute to the onset and progression of complex human diseases including neurodegenerative ones. Oxidative stress also is thought to be a common underlying mechanism that leads to cellular dysfunction and demise in PD. This study was aimed to assess the epigenetic fingerprint in PD experimental model through HDAC, PARP and activities oxidative stress markers. Materials and methods: The study was carried out on five rat groups, control group, Parkinsonism group, sodium butyrate group, two parkinson’s disease groups co-treated and post treated with sodium butyrate. Parkinsonism was induced by ip injection of paraquat. Laboratory measurements included serum 8-OHdG, MDA level as biomarkers of oxidative stress. HDAC and PARP activities were measured as other epigenetic mechanisms. Results: PD group, PD co-treated and post treated with sodium butyrate showed significant increase in HDAC and PARP activities. Also, there was significant increase in serum 8-OHdG level and MDA level in both serum and tissue. Conclusion and recommendations: The increments in HDAC and PARP activities are either two of the pathogenic mechanisms of the disease or it affords PD patients neuroprotection and benefits. Also, sodium butyrate is one of best antioxidant and neuroprotective agents. We recommended for further studies in HDAC and sodium butyrate as inhibitor in neurodegerative diseases, other diseases and normal state.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"11-20"},"PeriodicalIF":0.0,"publicationDate":"2015-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Winnie Thomas, Sireesha Divyakolu, V. Sreekanth, Vallomkonda Ramesh Om Sai, Vallomkonda Nagaratna, Q. Hasan, Y. R. Ahuja
Non-synonymous mutations/ polymorphism in amyloid precursor protein (APP) gene cause overproduction of Aβ proteins or affect its split into Aβ40 and Aβ42 peptides. Aβ42 has been considered to be a toxic peptide playing a major role in the pathogenesis of Alzheimers (AD). Similar APP plaques were observed in the brains of Down syndrome (DS) patients and high level of plasma APP was observed in patients with severe Autism spectrum Disorder (ASD). The aim of this study was to evaluate exon 16 and 17, the hotspot regions of APP gene in patients with neurobehavioral disorders like AD, DS and ASD. A total of 75 cases were recruited in the study which included AD (n=25), DS (n=25), and ASD (n=25). Polymerase chain reaction (PCR) analysis and sequencing was carried out using exon-intron encompassing primers for the selected APP gene regions. In-silico analysis was also carried out to identify the impact of sequence variants on the protein structure. Three exonic variants, two in exon 16: V683V, H684Y and one in exon 17, H733Q were identified in sporadic AD cases. Apart from these, two intronic variants were also observed. In-silico analysis showed that H733Q mutation may affect the structure and function of APP, whereas H684Y mutation is neutral. In an ASD case, our analysis showed an intronic variation ie. An A insertion at c.1964-13_1964-12insA. In-silico analysis predicted that this variation affects the elongation feature of the protein. None of the DS cases had any variation in this hotspot region. Our data indicate that variations in the selected hotspot region of APP may play an important role in the aetiology of neurobehavioral disorders.
{"title":"Variations in Hotspot Region of β-amyloid Precursor Protein (APP) Gene in Various Neurological Disorders from Hyderabad, a Cosmopolitan City of South India","authors":"Winnie Thomas, Sireesha Divyakolu, V. Sreekanth, Vallomkonda Ramesh Om Sai, Vallomkonda Nagaratna, Q. Hasan, Y. R. Ahuja","doi":"10.12691/IJCEN-3-1-2","DOIUrl":"https://doi.org/10.12691/IJCEN-3-1-2","url":null,"abstract":"Non-synonymous mutations/ polymorphism in amyloid precursor protein (APP) gene cause overproduction of Aβ proteins or affect its split into Aβ40 and Aβ42 peptides. Aβ42 has been considered to be a toxic peptide playing a major role in the pathogenesis of Alzheimers (AD). Similar APP plaques were observed in the brains of Down syndrome (DS) patients and high level of plasma APP was observed in patients with severe Autism spectrum Disorder (ASD). The aim of this study was to evaluate exon 16 and 17, the hotspot regions of APP gene in patients with neurobehavioral disorders like AD, DS and ASD. A total of 75 cases were recruited in the study which included AD (n=25), DS (n=25), and ASD (n=25). Polymerase chain reaction (PCR) analysis and sequencing was carried out using exon-intron encompassing primers for the selected APP gene regions. In-silico analysis was also carried out to identify the impact of sequence variants on the protein structure. Three exonic variants, two in exon 16: V683V, H684Y and one in exon 17, H733Q were identified in sporadic AD cases. Apart from these, two intronic variants were also observed. In-silico analysis showed that H733Q mutation may affect the structure and function of APP, whereas H684Y mutation is neutral. In an ASD case, our analysis showed an intronic variation ie. An A insertion at c.1964-13_1964-12insA. In-silico analysis predicted that this variation affects the elongation feature of the protein. None of the DS cases had any variation in this hotspot region. Our data indicate that variations in the selected hotspot region of APP may play an important role in the aetiology of neurobehavioral disorders.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"4-10"},"PeriodicalIF":0.0,"publicationDate":"2015-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Neuroprotective Role of Vitamin B 3 in Experimentally Induced Oxidative Stress","authors":"Afaf El Atrash, L. Dawood, E. Tousson, A. Salama","doi":"10.12691/IJCEN-3-1-4","DOIUrl":"https://doi.org/10.12691/IJCEN-3-1-4","url":null,"abstract":"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.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"3 1","pages":"21-25"},"PeriodicalIF":0.0,"publicationDate":"2015-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Epilepsy is a neuronal disorder that is observed globally but still it is not explored very well in most parts of the world. This disease is linked to different provocative causes and affects almost all generation, ethnicity and age population. Therefore, the aim of this article is to systemically review the literature about the prevalence, incidence and etiology of epilepsy to find possible approaches to control epilepsy. The worldwide prevalence of epilepsy is variable and varied among countries. High prevalence is found in adolescent and early age group population. In North America, Central and South America high prevalence is found in male except in New York, Bolivia, Honduras and Argentina where prevalence is high in female. In Asian countries such as China, India, Turkey and Saudi Arabia the prevalence is high in Male except in Pakistan here prevalence is high in female similarly to European countries where also prevalence is high in female. The prevalence of epilepsy in male and female is variable in African countries. Generalized seizure is high in America, Asia, Europe, and Africa than the other types of epilepsies. Very limited data is available about the incidence of epilepsy especially from low and lower middle income countries. The incidence rate of epilepsy is higher in the developing countries than the industrialized countries. Similarly, the incidence is also higher in male than female. Head injury, birth trauma, cerebrovascular disease, and intracranial infections (neurocysticercosis or meningoencephalitis) and genetic factors are the main causes of epilepsy.
{"title":"The Prevalence, Incidence and Etiology of Epilepsy","authors":"Shakirullah, N. Ali, A. Khan, Muhammad Nabi","doi":"10.12691/IJCEN-2-2-3","DOIUrl":"https://doi.org/10.12691/IJCEN-2-2-3","url":null,"abstract":"Epilepsy is a neuronal disorder that is observed globally but still it is not explored very well in most parts of the world. This disease is linked to different provocative causes and affects almost all generation, ethnicity and age population. Therefore, the aim of this article is to systemically review the literature about the prevalence, incidence and etiology of epilepsy to find possible approaches to control epilepsy. The worldwide prevalence of epilepsy is variable and varied among countries. High prevalence is found in adolescent and early age group population. In North America, Central and South America high prevalence is found in male except in New York, Bolivia, Honduras and Argentina where prevalence is high in female. In Asian countries such as China, India, Turkey and Saudi Arabia the prevalence is high in Male except in Pakistan here prevalence is high in female similarly to European countries where also prevalence is high in female. The prevalence of epilepsy in male and female is variable in African countries. Generalized seizure is high in America, Asia, Europe, and Africa than the other types of epilepsies. Very limited data is available about the incidence of epilepsy especially from low and lower middle income countries. The incidence rate of epilepsy is higher in the developing countries than the industrialized countries. Similarly, the incidence is also higher in male than female. Head injury, birth trauma, cerebrovascular disease, and intracranial infections (neurocysticercosis or meningoencephalitis) and genetic factors are the main causes of epilepsy.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"29-39"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hiba A Awooda, Gihan M. Sharara, N. Soltani, A. Saeed
Ischemic stroke usually initiates inflammation that potentiates neuronal death. The aim of this study was to evaluate the role of TNF-α and NF- қB in rats subjected to transient cerebral ischemia and to correlate their levels with the resulting of neurological deficits. Experimental procedures were performed on 30 adult male Wistar rats. In fifteen rats transient focal cerebral ischemia was induced by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24 hours (test group). Another 15 rats underwent the surgery at the same neck region without occlusion of CCA and served as a control group. Neurobehavioral assessments were evaluated. TNF-α was measured in the serum and brain tissue using ELISA method, and the expression of NF-қβ was done via western blotting as well. TNF-α concentration in both serum and brain tissue in the test group were significantly higher than control group (P < 0.001). The expression of NF- қB in the test group was significantly higher than control group (P < 0.001). Neurological deficit of the test group correlated negatively with both NF-қβ and TNF-α. Another positive correlation found between NF-қβ of the test group with the brain tissue and serum TNF-α. From the results of this study we can concluded that TNF-α and NF-қβ were significantly expressed in the affected brain tissue following cerebral ischemia/reperfusion in rats, with demonstration of a direct relationship between this inflammatory biomarkers and the consequent neurological deficits.
{"title":"Tumor Necrosis Factor-α and Nuclear Factor Kappa-β Expression in Rats Following Transient Focal Cerebral Ischemia Reperfusion","authors":"Hiba A Awooda, Gihan M. Sharara, N. Soltani, A. Saeed","doi":"10.12691/IJCEN-2-2-4","DOIUrl":"https://doi.org/10.12691/IJCEN-2-2-4","url":null,"abstract":"Ischemic stroke usually initiates inflammation that potentiates neuronal death. The aim of this study was to evaluate the role of TNF-α and NF- қB in rats subjected to transient cerebral ischemia and to correlate their levels with the resulting of neurological deficits. Experimental procedures were performed on 30 adult male Wistar rats. In fifteen rats transient focal cerebral ischemia was induced by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24 hours (test group). Another 15 rats underwent the surgery at the same neck region without occlusion of CCA and served as a control group. Neurobehavioral assessments were evaluated. TNF-α was measured in the serum and brain tissue using ELISA method, and the expression of NF-қβ was done via western blotting as well. TNF-α concentration in both serum and brain tissue in the test group were significantly higher than control group (P < 0.001). The expression of NF- қB in the test group was significantly higher than control group (P < 0.001). Neurological deficit of the test group correlated negatively with both NF-қβ and TNF-α. Another positive correlation found between NF-қβ of the test group with the brain tissue and serum TNF-α. From the results of this study we can concluded that TNF-α and NF-қβ were significantly expressed in the affected brain tissue following cerebral ischemia/reperfusion in rats, with demonstration of a direct relationship between this inflammatory biomarkers and the consequent neurological deficits.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"40-46"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66636261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trail making test (TMT) is one of the neuropsychological task to evaluate mental flexibility, visual search, motor speed and executive functions in neurological patients. Attention and speed are two mental functions necessary to complete the task in a short time with the least of errors. It is suggested that age and education have respectively positive and negative relationships with the time of performance of the task by neuropsychological patients. In this study it is hypothesized that (a) there is a positive relationship between education and motor speed in normal adults (b) there is a negative relationship can be seen between age and motor speed in normal adults and (c) normal men and women have not different motor speed in part A and part B of TMT. In order to do this study, 285 normal adults (men=112) were selected and their motor speed and errors were measured in part A and B. The results showed that (a) there was a negative, but not statistically significant, relationship between education and motor speed in groups, (b) there was a negative relationship between age and motor speed in part B only in male group, and (c) there was no differences between men and women in errors of part A and B, and there was no differences between them in motor speed in part A, but there was a significant difference in time of performance of part B. The results are discussed based on evidences of harder tasks in part B of TMT and gender differences in mental functions.
{"title":"Gender Differences in Trail Making Test Performance in a Nonclinical Sample of Adults","authors":"E. Foroozandeh","doi":"10.12691/IJCEN-2-1-1","DOIUrl":"https://doi.org/10.12691/IJCEN-2-1-1","url":null,"abstract":"Trail making test (TMT) is one of the neuropsychological task to evaluate mental flexibility, visual search, motor speed and executive functions in neurological patients. Attention and speed are two mental functions necessary to complete the task in a short time with the least of errors. It is suggested that age and education have respectively positive and negative relationships with the time of performance of the task by neuropsychological patients. In this study it is hypothesized that (a) there is a positive relationship between education and motor speed in normal adults (b) there is a negative relationship can be seen between age and motor speed in normal adults and (c) normal men and women have not different motor speed in part A and part B of TMT. In order to do this study, 285 normal adults (men=112) were selected and their motor speed and errors were measured in part A and B. The results showed that (a) there was a negative, but not statistically significant, relationship between education and motor speed in groups, (b) there was a negative relationship between age and motor speed in part B only in male group, and (c) there was no differences between men and women in errors of part A and B, and there was no differences between them in motor speed in part A, but there was a significant difference in time of performance of part B. The results are discussed based on evidences of harder tasks in part B of TMT and gender differences in mental functions.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lipocalin is a family of small molecules transporting extracellular proteins. Lipocalin-2 (LCN2) is a member of the family that sequesters iron-bound bacterial siderophores. The well-accepted function of LCN2 protein is its anti-bacterial behavior, however, its role in iron regulation, cellular migration, death and morphology modulation have been speculated. Several reports have correlated the presence of LCN2 in the infected, injured and stressed brain, and its effect in neuronal and non-neuronal cell types in the central nervous system. This article reviews studies that demonstrated mechanisms and functions of LCN2 expression in inflammed brain (acute and chronic), particularly in non-pathogen-associated neuroinflammation. This review predicts that LCN2 can be an attractive target to reduce mortality and morbidity associated with uncontrollable neuroinflammation.
{"title":"Lipocalin-2: a New Regulator of Non-Pathogen- Associated Neuroinflammation","authors":"Manoj Banjara","doi":"10.12691/IJCEN-2-1-3","DOIUrl":"https://doi.org/10.12691/IJCEN-2-1-3","url":null,"abstract":"Lipocalin is a family of small molecules transporting extracellular proteins. Lipocalin-2 (LCN2) is a member of the family that sequesters iron-bound bacterial siderophores. The well-accepted function of LCN2 protein is its anti-bacterial behavior, however, its role in iron regulation, cellular migration, death and morphology modulation have been speculated. Several reports have correlated the presence of LCN2 in the infected, injured and stressed brain, and its effect in neuronal and non-neuronal cell types in the central nervous system. This article reviews studies that demonstrated mechanisms and functions of LCN2 expression in inflammed brain (acute and chronic), particularly in non-pathogen-associated neuroinflammation. This review predicts that LCN2 can be an attractive target to reduce mortality and morbidity associated with uncontrollable neuroinflammation.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"8-15"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The aim of this study was to investigate the potential enhancement effects of resveratrol on the anticonvulsant effect of diazepam in pilocarpine induced seizures in rats. This study was carried out in 50 male albino rats subdivided into five equal groups; group1 received saline 0.9 % intraperitoneally and served as the control group; group 2 received pilocarpine; group 3 received resveratrol 30 min prior to pilocarpine; group 4 received diazepam 30 min prior to pilocarpine; group 5 received resveratrol/ diazepam combination 30 min prior to pilocarpine. Then, animals were decapitated and the hippocampus was collected and homogenized for determination of tissue interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), nitric oxide (NO), malondialdehyde level (MDA), superoxide dismutase (SOD) and catalase (CAT) activity. Resveratrol/diazepam combination produced significant decrease in tissue cytokines, NO and MDA while produced significant increase in tissue SOD and CAT activity compared to the use of diazepam alone. Also, this combination produced significant delay in the onset of convulsions and significant decrease in the mortality rates compared to the use of diazepam alone. In conclusion, resveratrol potentiates the anticonvulsant effect of diazepam and this may be beneficial in lowering the incidence of resistance to diazepam and also may allow reduction of its dose and side effects.
{"title":"Ameliorative Potential of Resveratrol on Experimentally-Induced Seizures","authors":"Ahmed M. Kabel","doi":"10.12691/IJCEN-2-2-1","DOIUrl":"https://doi.org/10.12691/IJCEN-2-2-1","url":null,"abstract":"The aim of this study was to investigate the potential enhancement effects of resveratrol on the anticonvulsant effect of diazepam in pilocarpine induced seizures in rats. This study was carried out in 50 male albino rats subdivided into five equal groups; group1 received saline 0.9 % intraperitoneally and served as the control group; group 2 received pilocarpine; group 3 received resveratrol 30 min prior to pilocarpine; group 4 received diazepam 30 min prior to pilocarpine; group 5 received resveratrol/ diazepam combination 30 min prior to pilocarpine. Then, animals were decapitated and the hippocampus was collected and homogenized for determination of tissue interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), nitric oxide (NO), malondialdehyde level (MDA), superoxide dismutase (SOD) and catalase (CAT) activity. Resveratrol/diazepam combination produced significant decrease in tissue cytokines, NO and MDA while produced significant increase in tissue SOD and CAT activity compared to the use of diazepam alone. Also, this combination produced significant delay in the onset of convulsions and significant decrease in the mortality rates compared to the use of diazepam alone. In conclusion, resveratrol potentiates the anticonvulsant effect of diazepam and this may be beneficial in lowering the incidence of resistance to diazepam and also may allow reduction of its dose and side effects.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"16-23"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alcohol abuse is a major causative factor of different neurological disorders, among which seizures and epilepsy have an important burden of disease. Through discussing different pathogenetic mechanisms, scholars have tried to define and describe the diversity of clinical pictures and occurrences that might elicit a convulsive disorder in the alcoholics. An overview of the history of the diagnostic and classificatory attempts is made in the present paper, and distinctions between acute intoxication and withdrawal syndromes are summarized. The influences of ethanol on the cellular level and on the synaptic processes are succinctly mentioned. The authors are focused predominantly in three particularities of the alcohol-related seizures, namely the so-called alcoholic epilepsy, withdrawal seizures, and subacute encephalopathy with seizures in chronic alcoholism (SESA syndrome). Several sources are quoted, and the paper contains a brief overview on the efficacy of benzodiazepines and other antiepileptic drugs in the treatment of this variety of clinical events.
{"title":"Alcohol Abuse and Seizures: an Overview of Clinical Notions and Pathogenetic Theories","authors":"G. Preçi, Gentian Vyshka","doi":"10.12691/IJCEN-2-1-2","DOIUrl":"https://doi.org/10.12691/IJCEN-2-1-2","url":null,"abstract":"Alcohol abuse is a major causative factor of different neurological disorders, among which seizures and epilepsy have an important burden of disease. Through discussing different pathogenetic mechanisms, scholars have tried to define and describe the diversity of clinical pictures and occurrences that might elicit a convulsive disorder in the alcoholics. An overview of the history of the diagnostic and classificatory attempts is made in the present paper, and distinctions between acute intoxication and withdrawal syndromes are summarized. The influences of ethanol on the cellular level and on the synaptic processes are succinctly mentioned. The authors are focused predominantly in three particularities of the alcohol-related seizures, namely the so-called alcoholic epilepsy, withdrawal seizures, and subacute encephalopathy with seizures in chronic alcoholism (SESA syndrome). Several sources are quoted, and the paper contains a brief overview on the efficacy of benzodiazepines and other antiepileptic drugs in the treatment of this variety of clinical events.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"153 1","pages":"4-7"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The role of TNF-α in ischemic/reperfusion (I/R) is still controversial. The aim of this study was to assess TNF-α in rats subjected to transient cerebral I/R and to correlate their levels with the resulting neurological deficits and oxidative stress biomarkers malondialdehyde and total antioxidant capacity (TAC). Material and Method: Experimental procedures were performed on 30 adult male Wistar rats. Divided into two groups fifteen rats in each, test group subjected to transient focal cerebral I/R by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24-hours. A control group underwent the surgery at the same neck region without occlusion of the CCA. Neurobehavioral assessments were evaluated. TNF-α was measured using ELISA method. Malondialdehyde and TAC were estimated colorimetry. Results: In the test group TNF-α and Malondialdehyde concentration in both serum and brain tissue were significantly higher than control group (P =0.000). In contrast, the serum and brain tissue levels of TAC in the test group was significantly lower compared to the sham operated rats (P = 0.000). The brain tissue and serum level of TNF-α were correlated negatively with neurological deficit and TAC and positively with Malondialdehyde (P = 0.000). Conclusion: the present study revealed a potential injurious role of TNF-α in rats subjected to cerebral I/R and demonstrated a direct relationship between TNF-α and oxidative stress biomarkers and the consequent neurological deficits.
{"title":"Tumor Necrosis Factor-α in Rats Following Transient Focal Cerebral Ischemia Reperfusion and Its Relation to Oxidative Stress","authors":"Hiba A Awooda, Gihan M. Sharara, S. A. Mahmoud","doi":"10.12691/IJCEN-2-2-2","DOIUrl":"https://doi.org/10.12691/IJCEN-2-2-2","url":null,"abstract":"Background: The role of TNF-α in ischemic/reperfusion (I/R) is still controversial. The aim of this study was to assess TNF-α in rats subjected to transient cerebral I/R and to correlate their levels with the resulting neurological deficits and oxidative stress biomarkers malondialdehyde and total antioxidant capacity (TAC). Material and Method: Experimental procedures were performed on 30 adult male Wistar rats. Divided into two groups fifteen rats in each, test group subjected to transient focal cerebral I/R by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24-hours. A control group underwent the surgery at the same neck region without occlusion of the CCA. Neurobehavioral assessments were evaluated. TNF-α was measured using ELISA method. Malondialdehyde and TAC were estimated colorimetry. Results: In the test group TNF-α and Malondialdehyde concentration in both serum and brain tissue were significantly higher than control group (P =0.000). In contrast, the serum and brain tissue levels of TAC in the test group was significantly lower compared to the sham operated rats (P = 0.000). The brain tissue and serum level of TNF-α were correlated negatively with neurological deficit and TAC and positively with Malondialdehyde (P = 0.000). Conclusion: the present study revealed a potential injurious role of TNF-α in rats subjected to cerebral I/R and demonstrated a direct relationship between TNF-α and oxidative stress biomarkers and the consequent neurological deficits.","PeriodicalId":75709,"journal":{"name":"Clinical and experimental neurology","volume":"2 1","pages":"24-28"},"PeriodicalIF":0.0,"publicationDate":"2014-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66635625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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