scholarly journals Investigation of the anticonvulsant and remyelinating potential of dexketoprofen on a rat model of primary generalized seizures

2020 ◽  
Vol 12 (4) ◽  
pp. 84-90
Author(s):  
O. A. Gromova ◽  
V. I. Demidov ◽  
A. G. Kalacheva ◽  
I. Yu. Torshin ◽  
T. R. Grishina ◽  
...  
Keyword(s):  
Rat Brain ◽  
Sodium Valproate ◽  
Rat Model ◽  
Histopathological Examination ◽  
Neuroprotective Effect ◽  
Albino Rats ◽  
Generalized Seizures ◽  
Seizure Model ◽  
The Brain ◽  
Anticonvulsant Effects

Objective: to investigate the effect of dexketoprofen on the severity of seizures on a rat model of primary generalized seizures caused by thiosemicarbazide; to evaluate the neuroprotective effect of the drug.Material and methods. The investigation was conducted on 72 male albino rats weighing 200–300 g. The animals were given dexketoprofen and/or comparison drugs (gabapentin, sodium valproate) for 5 days, after which the seizure model was reproduced. The effects of the drugs were evaluated from a set of neurological tests and the results of a histopathological examination of the brain.Results and discussion. Dexketoprofen reduced the severity, duration, and number of primary generalized seizures and potentiated the anticonvulsant effects of gabapentin and sodium valproate. Histopathological and morphometric examinations of the rat brain showed that dexketoprofen inhibited the formation of irreversible neuronal changes (27.2%; control, 55.7%), by transferring them into reversible changes (47.7%; control, 21.8%).Conclusion. The investigation made it possible to conclude that dexketoprofen had a moderate neuroprotective effect neurologically and morphometrically verified.

scholarly journals Carvedilol Exerts Neuroprotective Effect on Rat Model of Diabetic Neuropathy

2021 ◽  
Vol 12 ◽  
Author(s):  
Rania M. Magadmi ◽  
Mujahid A. Alsulaimani ◽  
Aziza R. Al-Rafiah ◽  
Muhammad Saeed Ahmad ◽  
Ahmed Esmat
Keyword(s):  
Oxidative Stress ◽  
Diabetic Neuropathy ◽  
Rat Model ◽  
Histopathological Examination ◽  
Neuroprotective Effect ◽  
Negative Control ◽  
Diabetic Patients ◽  
Sprague Dawley ◽  
Behavioural Tests ◽  
Diabetes Induction

Diabetic neuropathy (DN) commonly occurs in diabetics, affecting approximately 50% of both type 1 and 2 diabetic patients. It is a leading cause of non-traumatic amputations. Oxidative stress could play a key role in the pathophysiology of DN. This study aimed to investigate the potential neuroprotective effect of carvedilol on STZ-induced DN in rats. Thirty male Sprague Dawley rats (weighing 200–250 g) were randomly divided into five groups (six/group), where group 1 (negative control) received only the vehicle (0.5% of carboxymethyl cellulose orally 1 ml/kg). DN was induced by a single injection of remaining rats with streptozotocin (STZ; 50 mg/kg, i.p.). After diabetes induction, group 2 served as the diabetic untreated animals; while groups 3 and 4 were treated with carvedilol (1 and 10 mg/kg/d, orally, respectively). Group 5 received a-lipoic acid as a reference neuroprotective (100 mg/kg/d, orally). All treatments were continued for 45 days after diabetes induction, followed by behavioural tests. After sacrificing the animals, dorsal root ganglia, and sciatic nerves were collected for histopathological examination and biochemical assessments. Briefly, STZ administration caused cold allodynia, induced oxidative stress, and increased nerve growth factor (NGF) concentration. Nevertheless, carvedilol improved the behavioural tests, ameliorated the oxidative imbalance as manifested by reducing malondialdehyde, restoring glutathione content, and superoxide dismutase activity. Carvedilol also decreased NGF concentration in DRG homogenate. In conclusion, this study demonstrates the neuroprotective effect of carvedilol in an experimentally induced DN rat model through–at least partly–its antioxidant effect and reduced NGF concentration in DRG.

N-acetyl-l-cysteine attenuates oxidative damage and neurodegeneration in rat brain during aging

2018 ◽  
Vol 96 (12) ◽  
pp. 1189-1196 ◽  
Author(s):  
Geetika Garg ◽  
Sandeep Singh ◽  
Abhishek Kumar Singh ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Rat Brain ◽  
Neuroprotective Effect ◽  
Neuron Specific Enolase ◽  
Sirtuin 1 ◽  
Marker Genes ◽  
Aging Brain ◽  
Age Related ◽  
Nonenzymatic Antioxidants ◽  
Old Rats ◽  
The Brain

N-acetyl-l-cysteine (NAC) is a precursor of cysteine, which is known to increase the level of glutathione (GSH) in the brain. Several neurodegenerative changes linked to oxidative stress take place in the aging brain. This study aimed to assess the neuroprotective effect of NAC supplementation on age-dependent neurodegeneration in the rat brain. Young (4 months) and old (24 months) Wistar rats (n = 6 rats/group) were supplemented with NAC (100 mg/kg b.w. orally) for 14 days. Enzymatic and nonenzymatic antioxidants such as superoxide dismutase and catalase, and GSH and total thiol respectively, prooxidants such as protein carbonyl, advanced oxidation protein products, reactive oxygen species, and malondialdehyde were assessed in the brain homogenates. Furthermore, nitric oxide level, acetylcholinesterase activity, and Na+/K+–ATPase activity were measured and gene expression studies were also performed. The results indicated that NAC augmented the level of enzymatic and nonenzymatic antioxidants with a significant reduction in prooxidant levels in old rats. NAC supplementation also downregulated the expression of inflammatory markers (TNF-α, IL-1β, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats. The present findings support a neuroprotective role of NAC which has therapeutic implication in controlling age-related neurological disorders.

The beneficial effects of l-cysteine on brain antioxidants of rats affected by sodium valproate

2017 ◽  
Vol 36 (11) ◽  
pp. 1212-1221 ◽  
Author(s):  
RZ Hamza ◽  
NS El-Shenawy
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Protective Effect ◽  
Brain Tissue ◽  
Sodium Valproate ◽  
Histopathological Examination ◽  
Control Group ◽  
High Dose ◽  
Beneficial Effects ◽  
The Brain

Oxidative stress caused by sodium valproate (SV) is known to play a key role in the pathogenesis of brain tissue. The present study was designed to evaluate the protective effect of l-cysteine (LC) on the antioxidants of brain tissue of rats. The animals were divided into six groups: control group 1 was treated with saline as vehicle, groups 2 and 3 were treated with low and high doses of SV (100 and 500 mg/kg, respectively), group 4 was treated with LC (100 mg/kg), and groups 5 and 6 were treated with low-dose SV + LC and high-dose SV + LC, respectively. All the groups were treated orally by gastric tube for 30 successive days. Some antioxidant parameters were determined. Brain tissue (cerebral cortex) of SV-treated animals showed an increase in lipid peroxidation (LPO) and reduction in activity of enzymatic antioxidant and total antioxidant levels. Histopathological examination of cerebral cortex of SV rats showed astrocytic swelling, inflammation, and necrosis. After 4 weeks of the combination treatment of SV and LC daily, results showed significant improvement in the activity of cathepsin marker enzymes and restored the structure of the brain. LC was able to ameliorate oxidative stress deficits observed in SV rats. LC decreased LPO level and was also able to restore the activity of antioxidant enzymes as well as structural deficits observed in the brain of SV animals. The protective effect of LC in SV-treated rats is mediated through attenuation of oxidative stress, suggesting a therapeutic role for LC in individuals treated with SV.

scholarly journals Study of anticonvulsant activity of acetazolamide on albino rats and its influence on anticonvulsant activity of sodium valproate

2018 ◽  
Vol 7 (5) ◽  
pp. 976
Author(s):  
Hemanth Kumar K. H. ◽  
Kishore M. S.
Keyword(s):  
Body Weight ◽  
Sodium Valproate ◽  
Anticonvulsant Activity ◽  
Control Group ◽  
Albino Rats ◽  
Standard Group ◽  
Standard Drug ◽  
Male Sex ◽  
Seizure Model ◽  
Post Hoc

Background: Epilepsy is a common neurological disorder. 30-40% of patients will continue to have seizures despite the use of antiepileptic drugs either alone or in combination. The present study is undertaken to evaluate the anticonvulsant activity of Acetazolamide (ACZ) in albino rats and its influence on anticonvulsant activity of sodium valproate.Methods: Albino rats (150-200gms) of male sex were randomly selected, from central animal facility, MMCRI, Mysore. They were divided into 6groups (per model) of 6 rats each, control group-normal saline 0.5ml, standard group-sodium valproate (300mg/kg), dose 1-ACZ (8.75mg/kg), dose 2-ACZ (17.5mg/kg) and dose 3-ACZ (35mg/kg), dose 4-ACZ (8.75mg/kg) with sodium valproate (150mg/kg). The anti-convulsant activity was screened using MES model and PTZ model.Results: Results were analysed by ANOVA followed by post hoc Fisher’s LSD test. The ACZ has shown anticonvulsant activity at the dose of 17.5mg/kg and 35mg/kg body weight and combination of ACZ 8.75mg/kg with sodium valproate 150mg/kg both in MES model and PTZ model. The anticonvulsant activity of ACZ was less when compared to Sodium Valproate in both MES model and PTZ model. The anticonvulsant activity of combination, ACZ 8.75mg/kg with Sodium valproate 150mg/kg was comparable and more significant when compared to standard drug alone in MES model and PTZ model.Conclusions: The ACZ has shown anticonvulsant activity in MES model and PTZ induced seizure model of epilepsy. This study has shown that ACZ potentiated the effect of sodium valproate and can be used as add on drug with sodium valproate in epilepsy.

scholarly journals Neuroprotective Effect of Bean Phosphatidylserine on TMT-Induced Memory Deficits in a Rat Model

2020 ◽  
Vol 21 (14) ◽  
pp. 4901
Author(s):  
Minsook Ye ◽  
Bong Hee Han ◽  
Jin Su Kim ◽  
Kyungsoo Kim ◽  
Insop Shim
Keyword(s):  
Cognitive Function ◽  
Glucose Uptake ◽  
Rat Brain ◽  
Morris Water Maze ◽  
Rat Model ◽  
Water Maze ◽  
Neuroprotective Effect ◽  
Memory Function ◽  
Memory Deficits ◽  
Avoidance Task

Background: Trimethyltin (TMT) is a potent neurotoxin affecting various regions of the central nervous system, including the neocortex, the cerebellum, and the hippocampus. Phosphatidylserine (PS) is a membrane phospholipid, which is vital to brain cells. We analyzed the neuroprotective effects of soybean-derived phosphatidylserine (Bean-PS) on cognitive function, changes in the central cholinergic systems, and neural activity in TMT-induced memory deficits in a rat model. Methods: The rats were randomly divided into an untreated normal group, a TMT group (injected with TMT + vehicle), and a group injected with TMT + Bean-PS. The rats were treated with 10% hexane (TMT group) or TMT + Bean-PS (50 mg·kg−1, oral administration (p.o.)) daily for 21 days, following a single injection of TMT (8.0 mg/kg, intraperitoneally (i.p.)). The cognitive function of Bean-PS was assessed using the Morris water maze (MWM) test and a passive avoidance task (PAT). The expression of acetylcholine transferase (ChAT) and acetylcholinesterase (AchE) in the hippocampus was assessed via immunohistochemistry. A positron emission tomography (PET) scan was used to measure the glucose uptake in the rat brain. Results: Treatment with Bean-PS enhanced memory function in the Morris water maze (MWM) test. Consistent with the behavioral results, treatment with Bean-PS diminished the damage to cholinergic cells in the hippocampus, in contrast to those of the TMT group. The TMT+Bean-PS group showed elevated glucose uptake in the frontal lobe of the rat brain. Conclusion: These results demonstrate that Bean-PS protects against TMT-induced learning and memory impairment. As such, Bean-PS represents a potential treatment for neurodegenerative disorders, such as Alzheimer’s disease.

Effects of Acupuncture on Tissue-Oxygenation of the Rat Brain

1977 ◽  
Vol 05 (02) ◽  
pp. 147-154 ◽  
Author(s):  
Gregory S. Chen ◽  
Wilhelm Erdmann
Keyword(s):  
Rat Brain ◽  
Brain Tissue ◽  
Tissue Oxygenation ◽  
Perfusion Pressure ◽  
Tissue Perfusion ◽  
Albino Rats ◽  
Capillary Perfusion ◽  
Unconscious Patients ◽  
The Brain ◽  
Inspiratory Oxygen

Acupuncture has been claimed to be effective in restoring consciousness in some comatose patients. Possible mechanisms to explain alleged acupuncture-induced arousal may include vasodilatory effects caused by sympathetic stimulation which leads to an augmentation of cerebral microcirculation and thereby improves oxygen supply to the brain tissue. Experiments were performed in ten albino rats (Wistar) employing PO 2 microelectrodes which were inserted into the cortex of the animals through small burholes. Brain tissue PO 2 was continuously recorded before, during, and after acupuncture. Stimulation of certain acupuncture loci (Go-26) resulted in immediate increase of PO 2 in the frontal cortex of the rat brain. This effect was reproducible. The effect was comparable to that obtained with increase of inspiratory CO 2 known to induce arterial vasodilatation and thus capillary perfusion pressure. The effect was more significant as compared to tissue PO 2 increases obtained after increase of inspiratory oxygen concentration from 21% to 100%. It appears that acupuncture causes an increase of brain tissue perfusion which may be, at least in part, responsible for arousal of unconscious patients. Dilatation of cerebral vascular vessels and improvement of autoregulation in the brain by acupuncture stimulation may also explain the effectiveness of acupuncture in the treatment of migraine headache.

scholarly journals Histopathological and Biochemical Assessment of Neuroprotective Effects of Sodium Valproate and Lutein on the Pilocarpine Albino Rat Model of Epilepsy

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Aziza Rashed Al-Rafiah ◽  
Khlood Mohammed Mehdar
Keyword(s):  
Oxidative Stress ◽  
Sodium Valproate ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Latency Period ◽  
Cerebral Injury ◽  
Control Group ◽  
Rotarod Performance ◽  
Group I ◽  
Anti Inflammatory

Epilepsy is one of the most frequent neurological disorders characterized by an enduring predisposition to generate epileptic seizures. Oxidative stress is believed to directly participate in the pathways of neurodegenerations leading to epilepsy. Approximately, one-third of the epileptic patients who suffer from seizures do not receive effective medical treatment. Sodium valproate (SVP) is a commonly used antiepileptic drug (AED); however, it has toxic effects. Lutein (L), a carotenoid, has potent antioxidant and anti-inflammatory properties. The aim of this study was to determine the neuroprotective effect of sodium valproate (SVP) and lutein (L) in a rat model of pilocarpine- (PLC-) induced epilepsy. To achieve this aim, fifty rats were randomly divided into five groups. Group I: control, group II: received PLC (400 mg/kg intraperitoneally), group III: received PLC + SVP (500 mg/kg orally), group IV: received PLC + SVP + L (100 mg/kg orally), and group V: received (PLC + L). Racine Scale (RC) and latency period to onset seizure were calculated. After eight weeks, the hippocampus rotarod performance and histological investigations were performed. Oxidative stress was investigated in hippocampal homogenates. Results revealed that SVP and L, given alone or in combination, reduced the RC significantly, a significant delay in latency to PLC-kindling onset, and improved rotarod performance of rats compared with the PLC group. Moreover, L was associated with a reduction of oxidative stress in hippocampal homogenate, a significant decrease in serum tumor necrosis factor-alpha (TNF-α) level, and inhibition of cerebral injury and displayed antiepileptic properties in the PLC-induced epileptic rat model. Data obtained from the current research elucidated the prominent neuroprotective, antioxidant, and anti-inflammatory activities of lutein in this model. In conclusion, lutein cotreatment with AEDs is likely to be a promising strategy to improve treatment efficacy in patients suffering from epilepsy.

Uptake of Sodium Valproate and Effects on GABA Transport in Astroglial Primary Culture

1989 ◽  
Vol 16 (3) ◽  
pp. 244-247
Author(s):  
Michael Nilsson ◽  
Elisabeth Hansson ◽  
Lars Rönnbäck
Keyword(s):  
Valproic Acid ◽  
Cerebral Cortex ◽  
Sodium Valproate ◽  
Gaba Uptake ◽  
Newborn Rat ◽  
Gaba Transport ◽  
High Affinity ◽  
Major Factors ◽  
The Brain ◽  
Anticonvulsant Effects

The sodium salt of valproic acid (VPA) is an antiepileptic drug, which is effective in the treatment of several types of epilepsy. The drug has been postulated to exert its anticonvulsant effects by interaction with GABA-ergic systems in the brain. Results show a high-affinity uptake for sodium valproate in primary astroglial cultures from newborn rat cerebral cortex, with the kinetic parameters Km and Vmax not significantly different from those observed for GABA. This uptake was shown to interact with astroglial GABA transport in culture, with an increased Km value for GABA uptake. Since failure in GABA-ergic systems is postulated to be one of the major factors in the aetiology of epilepsy, it is interesting to note that the transport system for GABA in astrocytes is affected by sodium valproate.

scholarly journals Nanonaringenin and Vitamin E Ameliorate Some Behavioral, Biochemical, and Brain Tissue Alterations Induced by Nicotine in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Mohamed A. Kandeil ◽  
Eman T. Mohammed ◽  
Rania A. Radi ◽  
Fatma Khalil ◽  
Abdel-Razik H. Abdel-Razik ◽  
...  
Keyword(s):  
Vitamin E ◽  
Histopathological Examination ◽  
Behavioral Changes ◽  
Albino Rats ◽  
Cerebral Neurons ◽  
Short Memory ◽  
Prophylactic Use ◽  
Tissue Alterations ◽  
The Brain ◽  
Behavior And Cognition

Nicotine is the major alkaloid present in cigarettes that induces various biochemical and behavioral changes. Nanonaringenin (NNG) and vitamin E are antioxidants that are reported to mitigate serious impairments caused by some toxins and oxidants. Thus, we aimed to investigate the efficacy of NNG, vitamin E, and their combinations to ameliorate behavioral, biochemical, and histological alterations induced by nicotine in rats. Adult male albino rats were randomly grouped into six equal groups (10 rats/group): control, N (nicotine 1 mg/kg b.w./day S/C from 15th to 45th day, 5 days a week), NNG (25 mg/kg b.w./day orally for 45 days), N + NNG, N + E (nicotine + vitamin E 200 mg/kg b.w./day orally), and N + NNG + E (nicotine + NNG + vitamin E at the aforementioned doses). Behavioral tests were conducted on day 15 and 30 postnicotine injection, while memory tests, brain neurotransmitters, antioxidants, and histopathological examination were examined at day 30 only. As a result, nicotine impaired rats’ activity (hypoactivity and hyperactivity) and memory, induced anxiolytic and anxiogenic effects on rats, and altered neurotransmitters (acetylcholinesterase, serotonin, and dopamine), and redox markers (MDA, H2O2, GSH, and catalase) levels in brain homogenates. Thickening and congestion of the meninges and degeneration of the cerebral neurons and glia cells were observed. Cosupplementation with NNG, vitamin E, and their combination with nicotine was beneficial in the alleviation of activity impairments and improved short memory and cognition defects and exploratory behaviors. Our results indicate the antioxidant potential of NNG and vitamin E by modulating redox markers and neurotransmitters in the brain. Thus, data suggest that the prophylactic use of NNG, vitamin E, and/or their combination for (45 days) may have a successful amelioration of the disrupted behavior and cognition and biochemical and histopathological alterations induced by nicotine.

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