scholarly journals Behavioral, Biochemical and Histopathological effects of Standardised Pomegranate extract with Vinpocetine, Propolis or Cocoa in a rat model of Parkinson’s disease

2020 ◽  
Author(s):  
Azza A. Ali ◽  
Mona M. Kamal ◽  
Mona G. Khalil ◽  
Shimaa A. Ali ◽  
Hemat A. Elariny ◽  
...  
Keyword(s):  
Rat Model ◽  
Caspase 3 ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Acetylcholinesterase Activity ◽  
Brain Regions ◽  
Y Maze ◽  
Tnf Α ◽  
Locomotor Activities ◽  
Histopathological Effects

AbstractIntroductionParkinsonism is a neurodegenerative disorder. Pomegranate (POM) has been previously shown to have a dopaminergic neuroprotective effect against Parkinsonism.ObjectiveThe aim of the current study is to compare the efficacy of POM, vinpocetine, Propolis, Cocoa or L-dopa using RT-induced Parkinsonism rat model.MethodsRats were divided into seven groups; one normal and five RT model groups. One of the RT (2.5 mg/kg sc) groups served as non-treated parkinsonism model whereas the others were treated with either L-dopa (10 mg/kg PO) or with POM (150 mg/kg PO) together with each of the following; vinpocetine (VIN) (20 mg/kg PO), Propolis (300 mg/kg PO), Cocoa (24 mg/kg PO). Motor and cognitive performances were examined using three tests (catalepsy, open-field, Y-maze). Striatal dopamine, norepinephrine, serotonin, acetylcholinesterase, GABA, Glutamate, GSK 3B, BDNF levels were assessed as well as MDA, SOD, TAC, IL-1β, TNF-α, iNOs and caspase-3. Also, histopathological examinations of different brain regions were determined.ResultsTreatment with L-dopa alone or with all POM combination groups alleviated the deficits in locomotor activities, cognition, monoamine levels, acetylcholinesterase activity, oxidative stress, and inflammatory markers as well as caspase-3 expression induced by RT.ConclusionCombinations of POM with each of VIN, Propolis or Cocoa have a promising disease-modifying antiparkinsonian therapy even without being given as an adjuvant to L-dopa.

Neuroprotective effect of curcumin nanoparticles against rat model of status epilepticus induced by pilocarpine

2018 ◽  
Vol 15 (4) ◽  
Author(s):  
Yasser A. Khadrawy ◽  
Hussein G. Sawie ◽  
Eman N. Hosny
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Brain Regions ◽  
Necrosis Factor Alpha ◽  
Curcumin Nanoparticles ◽  
Tnf Α ◽  
Factor Alpha

Abstract Background The present study aims to investigate the neuroprotective effect of curcumin nanoparticles (Cur-NP) on the rat model of status epilepticus (SE) induced by pilocarpine. Methods In the present study, animals were divided into three groups: control animals, rat model of SE induced by a single dose of pilocarpine (380 mg/kg) injected intraperitoneally, and rat model of SE that received a daily intraperitoneal injection of Cur-NP (50 mg/kg) for four consecutive days prior to pilocarpine administration. Results The present results revealed a state of oxidative stress in the cortex and hippocampus of rat model of SE as compared to control. This was evident from the significant increase in lipid peroxidation and the significant decrease in reduced glutathione and nitric oxide. In addition, a significant increase in the levels of tumor necrosis factor-alpha (TNF-α) and caspase-3 was detected in the two studied brain regions of rat model of SE. The activities of acetylcholinesterase (AchE) and Na+/K+-ATPase decreased significantly in the cortex and hippocampus of rat model of SE. Protection with Cur-NP prevented oxidative stress and improved the elevated level of caspase-3 in the hippocampus and cortex and the hippocampal TNF-α to nonsignificant changes. Although Cur-NP prevented the decrease in AchE activity in the two studied brain regions, it failed to return Na+/K+-ATPase activity to its normal value. Conclusions It is clear from the present findings that Cur-NP could prevent the oxidative stress and neuroinflammation and cell death that were induced during SE. This in turn may help in ameliorating the subsequent cascades of events that follow SE and its development into epileptogenesis.

scholarly journals hUC-MSCs Exert a Neuroprotective Effect via Anti-apoptotic Mechanisms in a Neonatal HIE Rat Model

2019 ◽  
Vol 28 (12) ◽  
pp. 1552-1559 ◽  
Author(s):  
Jianwei Xu ◽  
Zhanhui Feng ◽  
Xianyao Wang ◽  
Ying Xiong ◽  
Lan Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Hypoxic Ischemic Encephalopathy ◽  
Human Umbilical Cord ◽  
Motor Functions ◽  
Ischemic Encephalopathy

In this study, we investigated how human umbilical cord mesenchymal stem cells exerted a neuroprotective effect via antiapoptotic mechanisms in a neonatal hypoxic-ischemic encephalopathy rat model. A total of 78 10-day old (P10) rats were used. After human umbilical cord mesenchymal stem cells were collected from human umbilical cords and amplified in culture, they were administered to rat subjects 1 h after induced hypoxic-ischemic encephalopathy treatment. The short-term (48 h) and long-term (28 day) outcomes were evaluated after human umbilical cord mesenchymal stem cells treatment using neurobehavioral function assessment. Triphenyltetrazolium chloride monohydrate staining was performed at 48 h. Beclin-2 and caspase-3 levels were evaluated with Western blot and real time polymerase chain reaction at 48 h. Human umbilical cord mesenchymal stem cells were collected and administrated to hypoxic-ischemic encephalopathy pups by intracerebroventricular injection. Hypoxic-ischemic encephalopathy typically induced significant delay in development and caused impairment in both cognitive and motor functions in rat subjects. Human umbilical cord mesenchymal stem cells were shown to ameliorate hypoxic-ischemic encephalopathy-induced damage and improve both cognitive and motor functions. Although hypoxic-ischemic encephalopathy induced significant expression of caspase-3 and Beclin-2, human umbilical cord mesenchymal stem cells decreased the expression of both of them. Human umbilical cord mesenchymal stem cells may serve as a potential treatment to ameliorate brain injury in hypoxic-ischemic encephalopathy patients.

scholarly journals Prenatal Zinc Supplementation Ameliorates Hippocampal Astrocytes Activation and Inflammatory Cytokines Expression Induced by Lipopolysaccharide in a Rat Model of Maternal Immune Activation

2021 ◽  
Author(s):  
Ebrahim Savareh ◽  
◽  
Nahid Davoodian ◽  
Ronak Mousaviyan ◽  
Maryam Ghasemi-Kasman ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Rat Model ◽  
Immune Activation ◽  
Zinc Supplementation ◽  
Neuroprotective Effect ◽  
Adult Offspring ◽  
Mrna Levels ◽  
Maternal Immune Activation ◽  
Tnf Α ◽  
Hippocampal Astrocytes

Objective: There is evidence that gestational exposure to lipopolysaccharide (LPS) results in fetal zinc deficiency, and eventually neurodevelopmental abnormalities. In this study, we utilized a rat model of maternal immune activation (MIA) to investigate the possible neuroprotective effect of zinc supplementation throughout pregnancy on hippocampal astrocytes activation as well as inflammatory cytokines expression in adult offspring. Methods: Pregnant rats received intraperitoneal injections of either LPS (0.5 mg/kg) or saline at gestational day (GD) 15 and 16 and orally gavaged with zinc sulfate (30 mg/kg) throughout pregnancy. Astrocyte density and histological assessment were evaluated in the hippocampus of adult offspring at postnatal day (PND) 60-62. Also, the mRNA levels of IL-6, TNF-α, IL-1β, NF-κB, and glial fibrillary acidic protein (GFAP) were measured using qPCR analysis. Results: Prenatal exposure to LPS resulted in up-regulated expression levels of IL-6, TNF-α, NF-κB, and GFAP in the hippocampus of adult pups. Moreover, offspring from LPS group showed an increased astrocyte density in CA1 region with no histological alterations in CA1 and CA3 areas. Conversely, maternal zinc supplementation ameliorated these inflammatory alterations induced by LPS. Discussion: This study provides support for the premise that zinc supplementation during pregnancy might be an early treatment option to inhibit hippocampal inflammation induced by the maternal immune response to infectious agents.

scholarly journals Neuroprotective Effect of Fisetin Through Suppression of IL-1R/TLR Axis and Apoptosis in Pentylenetetrazole-Induced Kindling in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Saima Khatoon ◽  
Nidhi Bharal Agarwal ◽  
Mohammed Samim ◽  
Ozair Alam
Keyword(s):  
Cytochrome C ◽  
Caspase 3 ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Seizure Threshold ◽  
Experimental Epilepsy ◽  
Kindling Model ◽  
Histological Alterations ◽  
Tnf Α ◽  
Cox 2

Epilepsy is a complex neurological disorder, characterized by frequent electrical activity in brain regions. Inflammation and apoptosis cascade activation are serious neurological sequelae during seizures. Fisetin (3, 3′,4′,7-tetrahydroxyflavone), a flavonoid molecule, is considered for its effective anti-inflammatory and anti-apoptotic properties. This study investigated the neuroprotective effect of fisetin on experimental epilepsy. For acute studies, increasing current electroshock (ICES) and pentylenetetrazole (PTZ)-induced seizure tests were performed to evaluate the antiseizure activity of fisetin. For the chronic study, the kindling model was established by the administration of PTZ in subconvulsive dose (25 mg/kg, i.p.). Mice were treated with fisetin (5, 10, and 20 mg/kg, p.o.) to study its probable antiseizure mechanism. The kindled mice were evaluated for seizure scores. Their hippocampus and cortex were assessed for neuronal damage, inflammation, and apoptosis. Histological alterations were observed in the hippocampus of the experimental mice. Levels of high mobility group box 1 (HMGB1), Toll-like receptor-4 (TLR-4), interleukin-1 receptor 1 (IL-1R1), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were assessed in the hippocampus and cortex by ELISA. The immunoreactivity and mRNA expressions of nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2), cytochrome C, and caspase-3 were quantified by immunohistochemical analysis and real-time PCR. Phosphorylation ELISA was performed to evaluate AkT/mTOR (mammalian target of rapamycin) activation in the hippocampus and cortex of the kindled mice. The results showed that fisetin administration increased the seizure threshold current (STC) in the ICES test. In PTZ-induced seizures, fisetin administration increased the latency for myoclonic jerks (MJs) and generalized seizures (GSs). In the PTZ-induced kindling model, fisetin administration dose-dependently suppressed the development of kindling and the associated neuronal damage in the experimental mice. Further, fisetin administration ameliorated kindling-induced neuroinflammation as evident from decreased levels of HMGB1, TLR-4, IL-1R1, IL-1β, IL-6, and TNF-α in the hippocampus and cortex of the kindled mice. Also, the immunoreactivity and mRNA expressions of inflammatory molecules, NF-κB, and COX-2 were decreased with fisetin administration in the kindled animals. Decreased phosphorylation of the AkT/mTOR pathway was reported with fisetin administration in the hippocampus and cortex of the kindled mice. The immunoreactivity and mRNA expressions of apoptotic molecules, cytochrome C, and caspase-3 were attenuated upon fisetin administration. The findings suggest that fisetin shows a neuroprotective effect by suppressing the release of inflammatory and apoptosis molecules and attenuating histological alterations during experimental epilepsy.

scholarly journals Neuroprotective effect of pterostilbene on ketamine induced schizophrenia in mice

2016 ◽  
Vol 1 (03) ◽  
pp. 96-103 ◽  
Author(s):  
Vasudha Bakshi ◽  
Devender Palsa ◽  
Nazia Begum ◽  
Jeevan Kommidi ◽  
Kapishwar Singh ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Open Field ◽  
Forced Swim Test ◽  
Neuroprotective Effect ◽  
Oxidant Stress ◽  
Acetylcholinesterase Activity ◽  
Control Group ◽  
Swim Test ◽  
Forced Swim ◽  
Y Maze

Objective: The aim of this study is to investigate the effects of pterostilbene on the behavior of mice and oxidative stress under the influence of Ketamine induced schizophrenia model. Methods: Schizophrenia was induced in mice by ketamine (50mg/kg/day, i.p, for 14 days). The treatment effect of pterostilbene (10 and 20 mg/kg/day, p.o, for 14 days) were verified on Actophotometer, Y-maze, Forced swim test (FST), open field apparatus, acetylcholinesterase activity and anti oxidant stress-related biomarker (Catalase, GSH, TBARS, SOD) levels in brain tissues. Results: Pterostilbene decreased TBARS, AChE and increased SOD, CAT, GSH levels in mice brain when compared with control group. It also improved spatial recognition memory, decreased mobility time, decreased exploratory behaviour and locomotor activity as evident by improved performance in Y-Maze task, Forced swim test, Open field test and Locomotor activity test. Conclusion: Pterostilbene has a neuroprotective role related atleast in part to an antioxidant mechanism and Anti AChE activity, which could be explored as more effective therapies of schizophrenia and other psychiatric diseases.

scholarly journals GLP-1 receptor agonist liraglutide has a neuroprotective effect on an aged rat model of Wolfram syndrome

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kadri Seppa ◽  
Maarja Toots ◽  
Riin Reimets ◽  
Toomas Jagomäe ◽  
Tuuliki Koppel ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Optic Nerve ◽  
Rat Model ◽  
Receptor Agonist ◽  
Neurodegenerative Disorder ◽  
Ganglion Cells ◽  
Neuroprotective Effect ◽  
Wolfram Syndrome ◽  
Retinal Ganglion ◽  
Knock Out

Abstract Wolfram syndrome (WS) is a rare neurodegenerative disorder that is mainly characterized by diabetes mellitus, optic nerve atrophy, deafness, and progressive brainstem degeneration. Treatment with GLP-1 receptor agonists has shown a promising anti-diabetic effect in WS treatment in both animal models and in human patients. Since previous research has tended to focus on investigation of the WS first symptom, diabetes mellitus, the aim of the present study was to examine liraglutide effect on WS-associated neurodegeneration. We took 9-month-old Wfs1 knock-out (KO) animals that already had developed glucose intolerance and treated them with liraglutide for 6 months. Our research results indicate that 6-month liraglutide treatment reduced neuroinflammation and ameliorated endoplasmic reticulum (ER) stress in the inferior olive of the aged WS rat model. Liraglutide treatment also protected retinal ganglion cells from cell death and optic nerve axons from degeneration. According to this, the results of the present study provide novel insight that GLP-1 receptor agonist liraglutide has a neuroprotective effect in the WS rat model.

Cordycepin Exerts Neuroprotective Effects via an Anti-Apoptotic Mechanism based on the Mitochondrial Pathway in a Rotenone-Induced Parkinsonism Rat Model

2019 ◽  
Vol 18 (8) ◽  
pp. 609-620 ◽  
Author(s):  
Xin Jiang ◽  
Pei-Chen Tang ◽  
Qin Chen ◽  
Xin Zhang ◽  
Yi-Yun Fan ◽  
...  
Keyword(s):  
Rat Model ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Dopamine Neurons ◽  
Substantia Nigra Pars Compacta ◽  
Neuroprotective Effects ◽  
Cyt C

Background: Cordycepin (Cor), one of the major bioactive components of the traditional Chinese medicine Cordyceps militaris, has been used in clinical practice for several years. However, its neuroprotective effect remains unknown. Aim: The purpose of the study was to evaluate the neuroprotective effects of Cor using a rotenoneinduced Parkinson’s Disease (PD) rat model and to delineate the possible associated molecular mechanisms. Methods: In vivo, behavioural tests were performed based on the 10-point scale and grid tests. Levels of dopamine and its metabolites in the striatum and the numbers of TH-positive neurons in the Substantia Nigra pars compacta (SNpc) were investigated by high-performance liquid chromatography with electrochemical detection and immunohistochemical staining, respectively. In vitro, cell apoptosis rates and Mitochondrial Membrane Potential (MMP) were analysed by flow cytometry and the mRNA and protein levels of Bax, Bcl-2, Bcl-xL, Cytochrome c (Cyt-c), and caspase-3 were determined by quantitative real-time PCR and western blotting. Results: Showed that Cor significantly improved dyskinesia, increased the numbers of TH-positive neurons in the SNpc, and maintained levels of dopamine and its metabolites in the striatum in rotenone- induced PD rats. We also found that apoptosis was suppressed and the loss of MMP was reversed with Cor treatment. Furthermore, Cor markedly down-regulated the expression of Bax, upregulated Bcl-2 and Bcl-xL, inhibited the activation of caspase-3, and decreased the release of Cyt-c from the mitochondria to the cytoplasm, as compared to those in the rotenone-treated group. Conclusion: Therefore, Cor protected dopamine neurons against rotenone-induced apoptosis by improving mitochondrial dysfunction in a PD model, demonstrating its therapeutic potential for this disease.

Neuroprotective effect of hydroxy safflor yellow A against cerebral ischemia-reperfusion injury in rats: putative role of mPTP

2016 ◽  
Vol 27 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Sruthi Ramagiri ◽  
Rajeev Taliyan
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Radical Scavenger ◽  
Neuroprotective Effects ◽  
Y Maze ◽  
Tnf Α

AbstractHydroxy safflor yellow A (HSYA) has been translated clinically for cardiovascular diseases. HSYA is also greatly acknowledged for its protective effects against cerebral ischemic-reperfusion (I/R) injury. Although the precise mechanism of cerebral I/R injury is not fully understood, oxygen-derived free radicals and mitochondrial permeability transition pore (mPTP) opening during I/R injury are widely recognized as an important contributor to neuronal injury. Thus, we speculated that the neuroprotective effects of HSYA against cerebral I/R injury may be associated with mPTP modulation.Induction of I/R injury was achieved by 60 min of middle cerebral artery occlusion, followed by reperfusion for 24 h. For behavior and cognitive assessment, neurological scoring (NSS), rotarod, and Y-maze task were performed. Oxidative damage was measured in terms of markers such as malondialdehyde, reduced glutathione, and catalase levels and cerebral infarct volumes were quantified using 2,3,5-triphenyl tetrazolinium chloride staining. I/R injury-induced inflammation was determined using tumor necrosis factor-α (TNF-α) levels.Animals exposed to I/R injury showed neurological severity, functional and cognitive disability, elevated oxidative markers, and TNF-α levels along with large infarct volumes. HSYA treatment during onset of reperfusion ameliorated performance in NSS, rotarod and Y-maze attenuated oxidative damage, TNF-α levels, and infarction rate. However, treatment with carboxyatractyloside, an mPTP opener, 20 min before HSYA, attenuated the protective effect of HSYA.Our study confirmed that protective effect of HSYA may be conferred through its free radical scavenger action followed by inhibiting the opening of mPTP during reperfusion and HSYA might act as a promising therapeutic agent against cerebral I/R injury.

scholarly journals Neuroprotective Effect of Curcumin on the Nigrostriatal Pathway in a 6-Hydroxydopmine-Induced Rat Model of Parkinson’s Disease is Mediated by α7-Nicotinic Receptors

2020 ◽  
Vol 21 (19) ◽  
pp. 7329
Author(s):  
Eslam El Nebrisi ◽  
Hayate Javed ◽  
Shreesh K Ojha ◽  
Murat Oz ◽  
Safa Shehab
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Dopaminergic Neurons ◽  
Motor Behavior ◽  
Neurodegenerative Disorder ◽  
Neuroprotective Effect ◽  
Intraperitoneal Administration ◽  
Neuroprotective Effects ◽  
Α7 Nachr

Parkinson’s disease (PD) is a common neurodegenerative disorder, characterized by selective degeneration of dopaminergic nigrostriatal neurons. Most of the existing pharmacological approaches in PD consider replenishing striatal dopamine. It has been reported that activation of the cholinergic system has neuroprotective effects on dopaminergic neurons, and human α7-nicotinic acetylcholine receptor (α7-nAChR) stimulation may offer a potential therapeutic approach in PD. Our recent in-vitro studies demonstrated that curcumin causes significant potentiation of the function of α7-nAChRs expressed in Xenopus oocytes. In this study, we conducted in vivo experiments to assess the role of the α7-nAChR on the protective effects of curcumin in an animal model of PD. Intra-striatal injection of 6-hydroxydopmine (6-OHDA) was used to induce Parkinsonism in rats. Our results demonstrated that intragastric curcumin treatment (200 mg/kg) significantly improved the abnormal motor behavior and offered neuroprotection against the reduction of dopaminergic neurons, as determined by tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra and caudoputamen. The intraperitoneal administration of the α7-nAChR-selective antagonist methyllycaconitine (1 µg/kg) reversed the neuroprotective effects of curcumin in terms of both animal behavior and TH immunoreactivity. In conclusion, this study demonstrates that curcumin has a neuroprotective effect in a 6-hydroxydopmine (6-OHDA) rat model of PD via an α7-nAChR-mediated mechanism.

scholarly journals Effect of Glycyrrhizic Acid on Scopolamine-Induced Cognitive Impairment in Mice

2020 ◽  
Vol 24 (Suppl 1) ◽  
pp. S48-55
Author(s):  
Ju Yeon Ban ◽  
Hyun Kyung Park ◽  
Su Kang Kim
Keyword(s):  
Superoxide Dismutase ◽  
Cognitive Impairment ◽  
Glycyrrhizic Acid ◽  
Neuroprotective Effect ◽  
Acetylcholinesterase Activity ◽  
Treated Group ◽  
Glycyrrhiza Uralensis ◽  
Mice Model ◽  
Maze Test ◽  
Y Maze

Purpose: Cognitive impairment is one of the main symptoms of Alzheimer disease and other dementias. Glycyrrhiza uralensis is a natural product that has a protective effect against cognitive impairment. In this study, we investigated whether glycyrrhizic acid, among the main bioactive components of <i>Glycyrrhiza uralensis</i>, has a neuroprotective effect on scopolamine-induced cognitive impairment.Methods: Twenty-week-old male Institute of Cancer Research mice were used in this study. The scopolamine-induced cognitive impairment mice model was used. Glycyrrhizic acid was orally administered to mice once daily for 21 days, while scopolamine (1 mg/kg) treatment was delivered 30 minutes before behavioral tests. Donepezil (2 mg/kg) was used as a positive drug control. To evaluate the effect of glycyrrhizic acid, the following assessments were performed on hippocampal tissue: Y-maze test, acetylcholinesterase activity, antioxidant enzymes’ activity (superoxide dismutase, catalase). Western blotting for phosphor-extracellular signal-regulated kinase, P38, and c-Jun NH2-terminal kinase was conducted.Results: We found that glycyrrhizic acid administration significantly improved scopolamine-induced cognitive impairment in the Y-maze test. The acetylcholinesterase activity, superoxide dismutase, and catalase activity in the glycyrrhizic acid-treated group showed a significant reversal of cognitive impairment compared with the scopolamine-treated group.Conclusions: Our results suggest that glycyrrhizic acid has a neuroprotective effect on cognitive function in scopolamine-induced cognitive impairment.

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