scholarly journals NEUROPROTECTIVE EFFECTS OF POMEGRANATE JUICE ON LEAD INDUCED NEUROTOXICITY IN MICE

2017 ◽  
Vol 9 (2) ◽  
pp. 207
Author(s):  
Leila Gadouche ◽  
Noureddine Djebli ◽  
Khayra Zerrouki
Keyword(s):  
Drinking Water ◽  
Cerebral Cortex ◽  
Lead Acetate ◽  
Neuronal Degeneration ◽  
Neuroprotective Effect ◽  
Pomegranate Juice ◽  
Total Phenolic ◽  
Control Group ◽  
Histological Structure ◽  
Neuroprotective Effects

<p><strong>Objective: </strong>This study evaluates the potential neuroprotective of the pomegranate juice against chronic intoxication with lead acetate for 3<strong> </strong>months.</p><p><strong>Methods: </strong>Twenty-one female Swiss mice divided into 3 groups were employed in the present investigation. Control group: received drinking water for 90 days, neurotoxic group were exposed to 1000 ppm of lead acetate in the drinking water for 12 weeks, and neurotoxic treated group represents the mice received treatment with juice pomegranate diluted with distilled water (v/v) orally for 4 h / day followed by lead acetate at a dose of 1000 ppm orally for 20 h / day for 90 days. After cessation of treatment, neurobehavioral studies using the open field test, black and white test box and swimming test were made. In the next phase, brain injury was assessed histologically with hematoxylin-eosin staining.</p><p><strong>Results:</strong> Chronic exposure to lead led to significant increase in the level of anxiety, depression and the locomotor activity (P &lt; 0.05). It was confirmed by histopathological alterations in many areas of the cerebral cortex and hippocampus including neuronal degeneration and decrease cell density. Treatment with the juice significantly improve the level of depression, locomotor function (P &lt; 005) and anxiety (P &gt; 0.05) in mice exposed to lead as well as restored the histological structure in cerebral cortex and hippocampus of mice. The total phenolic and flavonoids content in juice of pomegranate was found to be 3809. 8±29.404 mg GAE/l; 2109. 57±18.936 mg QE /l of juice.</p><p><strong>Conclusion: </strong>This finding suggests that phenolic compounds found in pomegranate juice provide a neuroprotective effect on behavioural impairments and histopathological change induced by lead.</p>

Neuroprotective Activity of the Methanolic Extract of Indigofera aspalathoides against Scopalamine induced Alzheimer's Disease in Experimental Rats

2021 ◽  
pp. 5163-5168
Author(s):  
Rajaram C. ◽  
S. Nelson Kumar ◽  
S. S. Sheeba Tabassum ◽  
Manohar R. ◽  
Sumanjali C.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traditional Medicine ◽  
Methanolic Extract ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Neuroprotective Activity ◽  
Control Group ◽  
Histological Structure ◽  
Anticancer Activities

The plant Indigofera aspalathoides is a traditional medicine with tremendous therapeutic potential which finds it use in treatment of various ailments such as antibacterial, antioxidant, anti-inflammatory, antidiabetic, and anticancer activities. There are no reports that related to the use of this plant in treating patients with Alzheimer’s disease (AD). Hence present study was aimed to scientifically evaluate the neuroprotective effect of the methanolic extract of Indigofera aspalathoides against scopalamine induced Alzheimer’s disease in experimental rats using behavioral tests like elevated plus maze, Y-maze, and rota-rod tests. In addition to this, biochemical evaluation for acetylcholinesterase activity and histopathological evaluation of brain were done. The results suggests that methanolic extract Indigofera aspalathoides (200mg/kg B.wt and 400mg/kg B.wt) used in this study shows significant improvement of various behavioral parameters like locomotion, anxiety, memory, motor integrity and coordination etc when compared to control group. MEIA inhibited brain AChE enzyme, thereby elevating Ach concentration in brain homogenate and ultimately improved memory of rats. Further, more or less normal histological structure of the hippocampus and all amyloid plaques and neurofibrillary tangles that are formed under the influence of scopolamine disappeared in the rats pretreated with MEIA (200mg/kg B.wt and 400mg/kg B.wt). It can be concluded that our results strongly support the anti-Alzheimer’s potential of the methanolic extract of the plant I.aspalathoides and its use in traditional medicine.

scholarly journals Anticonvulsant and Neuroprotective Activities ofPhragmanthera austroarabicaExtract in Pentylenetetrazole-Kindled Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Hibah M. Aldawsari ◽  
Basma G. Eid ◽  
Thikrayat Neamatallah ◽  
Sawsan A. Zaitone ◽  
Jihan M. Badr
Keyword(s):  
Plant Extract ◽  
Hippocampal Neurons ◽  
Seizure Activity ◽  
Chemical Constituents ◽  
Neuroprotective Effect ◽  
Intraperitoneal Administration ◽  
Neuroprotective Activity ◽  
Total Phenolic ◽  
Control Group ◽  
Phenolic Contents

Anticonvulsant and neuroprotective activity ofPhragmanthera austroarabicaextract were tested in pentylenetetrazole-kindled mice. All the chemical constituents of the plant extract were identified. Additionally, the extract was standardized and proved to contain total phenolic contents equal to379.92±1.32 mg gallic acid equivalents/g dry plant extract. Induction of kindling was achieved by repeated intraperitoneal administration of pentylenetetrazole (35 mg/kg) twice weekly. Male albino mice were givenP.austroarabicaextract (200, 400, or 800 mg/kg). The two higher doses (400 or 800 mg/kg) of the extract significantly caused notable reduction in seizure activity and hippocampal malondialdehyde level compared to pentylenetetrazole control group. The highest dose enhanced cortical GSH level and showed intact DNA in the laddering assay. Upon studying the neuroprotective effect, mice treated with the higher dose of the extract demonstrated an improvement in the percent of surviving neurons in the cortex and hippocampus. We concluded thatP. austroarabicaextract ameliorated seizure activity and protected cortical and hippocampal neurons against pentylenetetrazole-induced kindling in mice.

scholarly journals Impact of lead acetate and sodium and potassium stearates on lipid peroxidation processes in the body of experimental animals

2021 ◽  
Vol 100 (4) ◽  
pp. 406-410
Author(s):  
Olha Ye. Fedoriv ◽  
Alexandra Ye. Kopach ◽  
Nataliia A. Melnyk
Keyword(s):  
Lipid Peroxidation ◽  
Drinking Water ◽  
Lead Acetate ◽  
Sodium Stearate ◽  
The Body ◽  
Female Rats ◽  
White Female ◽  
Control Group ◽  
Diene Conjugates ◽  
Group 2

Introduction. Given the significant prevalence of lead in the environment, research in this area has significant social and economic importance. Lead compounds are characterized by high toxicity and increased ability to cumulate in ecosystems, humans, and animals. Lead enters the human body with food, drinking water, atmospheric air, and smoking. Lead causes pathological changes in the nervous system, blood-forming organs, kidneys, etc. Materials and methods. The experiments were carried out on four groups of white female rats, each included seven animals, weighing 150-200 g. The first group of animals was a control. The second group consumed dechlorinated water from the city water supply, followed by lead acetate. The animals from the third and fourth groups drank the same water with sodium stearate and potassium stearate content in a dose of 1/250 LD50. After the 40th-day of the use of these waters, the animals were orally administered lead acetate at a dose of 7 mg/kg. The levels of lipid peroxidation biomarkers were studied by studying the content of diene conjugates (DC) and malondialdehyde (MDA) in blood serum, liver, and kidney homogenates. Results. The administration of 1/2 acetate LD50 to lead in experimental rats drinking water with stearates was accompanied by a significant increase in the DCs concentration and (MDA) in animals. Higher concentrations of LPO products were observed in the group of animals that consumed water from potassium stearate. Conclusions. 1. With the oral administration of lead acetate against the background of drinking water containing stearates at a dose of 1/250 LD50, an increase in lipid peroxidation indices was noted compared with the control group. 2. Higher concentrations of LPO products were observed in the group of animals consuming water from potassium stearate.

scholarly journals Vasculoprotective and Neuroprotective Effects of Various Parts of Pomegranate: In Vitro, In Vivo, and Preclinical Studies

2021 ◽  
Author(s):  
Maria Trapali ◽  
Vasiliki Lagouri
Keyword(s):  
Ellagic Acid ◽  
Therapeutic Agent ◽  
Neuroprotective Effect ◽  
Pomegranate Juice ◽  
In Vivo Studies ◽  
Neuroprotective Effects ◽  
Hydrolysable Tannins ◽  
Main Components

Pomegranate (Punica granatum L.) is one of the oldest edible fruits in the Mediterranean area and has been used extensively in the folk medicine. Popularity of pomegranate has increased especially in the last decade because of the health effects of the fruit. Polyphenols, represent the predominant class of phytochemicals of pomegranate, mainly consisting of hydrolysable tannins and ellagic acid. Pomegranate is a rich source of the ellagitannin punicalagin, which has aroused considerable interest in pomegranate fruit as a new therapeutic agent in recent years. Most studies on the effects of pomegranate juice have focused on its ability to cure diabetes and atherosclerosis. The present review summarizes some recent studies on the vasculoprotective and neuroprotective effect of various parts of pomegranate and its main compounds especially hydrolysable tannins ellagitannins, ellagic acid and their metabolites. The in vitro and in vivo studies, showed that the whole parts of pomegranate as well as its main components had a positive influence on blood glucose, lipid levels, oxidation stress and neuro/inflammatory biomarkers. They could be used as a future therapeutic agent towards several vascular and neurodegenerative disorders such as hypertension, coronary heart disease and Alzheimer.

Cytoprotective Effects of Zingiber officinale Against the Oxidative Stress Induced by Lead Acetate Toxicity in Rats

2020 ◽  
Author(s):  
O. Aouacheri ◽  
S. Saka
Keyword(s):  
Oxidative Stress ◽  
Drinking Water ◽  
Lead Acetate ◽  
Zingiber Officinale ◽  
Treated Group ◽  
Normal Diet ◽  
Male Rats ◽  
Control Group ◽  
Experimental Diet ◽  
Group I

The evaluation of the effect of ginger on the modulation of toxic effects induced by lead is the objective of our study. Forty male rats were randomly divided into four groups and treated daily for 3 consecutive months. Group I (0-0) was kept as control; group II (0-G) received an experimental diet with 2% of ginger; group III (Pb-0) received 2% lead acetate dissolved in drinking water with a normal diet; and group IV (Pb-G) received 2% lead acetate in drinking water and an experimental diet containing 2% ginger. Lead acetate exposure caused a significant increase of organosomatic indexes, hepatic, lipid, and urine profiles. In addition, lead acetate has a pro-oxidative effect expressed by a significant decrease in tissue GSH levels and the enzymatic activity of GPx and CAT. This pro-oxidative action was also marked by an increase in MDA level and GST activity in lead-treated group. Feeding ginger-supplemented diet to lead acetate-treated rats restored all the parameters studied as compared to control. These results suggest that ginger treatment exerts a protective effect on metabolic disorders by decreasing the oxidative stress.

scholarly journals Phytochemical Composition, Antioxidant Activity, and Neuroprotective Effect ofTerminalia chebulaRetzius Extracts

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Chia Lin Chang ◽  
Che San Lin
Keyword(s):  
Antioxidant Activity ◽  
Methanol Extract ◽  
Antioxidant Activities ◽  
Neuroprotective Effect ◽  
Water Extract ◽  
Ethanol Extract ◽  
Total Phenolic ◽  
Cupric Sulfate ◽  
Neuroprotective Effects

The objectives of this study were to determine phytochemical compositions, chemiluminescence antioxidant activities, and neuroprotective effects on PC12 cells for water, methanol, and 95% ethanol extracts of the air-dried fruit ofTerminalia chebulaRetzius. The water extract afforded the greatest yield, and total phenolic and tannin content. The methanol extract yielded the greatest total triterpenoid content. Based on four chemiluminescence antioxidant assays, the three extracts showed various degrees of antioxidant activity. The methanol extract showed good antioxidant activity based on the horseradish peroxidase-luminol-hydrogen peroxide (H2O2) assay. The water extract appeared to have good antioxidant activities in cupric sulfate-Phen-Vc-H2O2and luminol-H2O2assays. Pyrogallol-luminol assay showed the 95% ethanol extract to have good antioxidant activity. The methanol and water extracts presented neuroprotective activities on H2O2-induced PC12 cell death at 0.5–5.0 μg/mL. Further investigations are necessary to verify these activitiesin vivo.

scholarly journals Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guangqian Li ◽  
LeiQian ◽  
Pan Gu ◽  
Dan Fan
Keyword(s):  
Cardiac Arrest ◽  
Neuroprotective Effect ◽  
Serum Levels ◽  
Spontaneous Circulation ◽  
Cerebral Injury ◽  
Control Group ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Neuroprotective Effects ◽  
Return Of Spontaneous Circulation

Abstract Background Neuroprotection strategies after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR) remain key areas of basic and clinical research. This study was designed to investigate the neuroprotective effects of dexmedetomidine following resuscitation and potential mechanisms. Methods Anesthetized rats underwent 6-min asphyxia-based cardiac arrest and resuscitation, after which the experimental group received a single intravenous dose of dexmedetomidine (25 μg/kg). Neurological outcomes and ataxia were assessed after the return of spontaneous circulation. The serum levels and brain expression of inflammation markers was examined, and apoptotic cells were quantified by TUNEL staining. Results Neuroprotection was enhanced by dexmedetomidine post-conditioning after the return of spontaneous circulation. This enhancement was characterized by the promotion of neurological function scores and coordination. In addition, dexmedetomidine post-conditioning attenuated the serum levels of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α at 2 h, as well as interleukin IL-1β at 2, 24, and 48 h. TUNEL staining showed that the number of apoptotic cells in the dexmedetomidine post-conditioning group was significantly reduced compared with the control group. Further western blot analysis indicated that dexmedetomidine markedly reduced the levels of caspase-3 and nuclear factor-kappa B (NF-κB) in the brain. Conclusions Dexmedetomidine post-conditioning had a neuroprotective effect against cerebral injury following asphyxia-induced cardiac arrest. The mechanism was associated with the downregulation of apoptosis and neuroinflammation.

scholarly journals Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

2021 ◽  
Author(s):  
Yasaman Razavi ◽  
Fariborz Keyhanfar ◽  
Abbas Haghparast ◽  
Ronak Shabani ◽  
Mehdi Mehdizadeh
Keyword(s):  
Dentate Gyrus ◽  
Chronic Exposure ◽  
Neuronal Degeneration ◽  
Hippocampal Neurogenesis ◽  
Control Group ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Ki 67 ◽  
Promising Therapeutic Approach ◽  
Abstinence Period

Abstract Chronic methamphetamine (meth) abuse can lead to certain deficits in the hippocampal function by affecting the hippocampal neurogenesis and plasticity. To determine whether cannabidiol (CBD) can promote proliferation and maturation of neuronal progenitor cells, this study investigated the CBD effect on neurogenesis in the hippocampal dentate gyrus (DG) following chronic exposure to meth in rats. The rats received 2 mg/kg of meth twice a day for ten days. Next, immunofluorescence was performed to evaluate the effect of intracerebroventricular (ICV) administration of CBD (50 µg/5 µL) over an abstinence period (ten days) on the expression levels of neurogenesis markers, such as Ki67, NeuN, and doublecortin (DCX). Moreover, neuronal degeneration in the hippocampus was assessed using Nissl staining. According to our findings, repeated ICV administration of CBD improved cell proliferation and neurogenesis and increased the number of Ki-67 and DCX-positive cells in the abstinence period. Meanwhile, meth treatment subjects caused a significant decrease in the number of neurogenesis makers, as compared to the control group. The neurogenesis markers (Ki-67 and DCX) could be somewhat reversed, while NeuN did not show any significant increase in the CBD group. Our findings demonstrated that CBD can induce neuroprotective effects by modulating neurogenesis. Therefore, it can provide a promising therapeutic approach to improve cognitive performance following chronic exposure to psychostimulant drugs, including meth.

scholarly journals Neuroprotective Effect of Chronic Intracranial Toxoplasma gondii Infection in a Mouse Cerebral Ischemia Model

2020 ◽  
Vol 58 (4) ◽  
pp. 461-466
Author(s):  
Seung Hak Lee ◽  
Bong-Kwang Jung ◽  
Hyemi Song ◽  
Han Gil Seo ◽  
Jong-Yil Chai ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Toxoplasma Gondii ◽  
Neuroprotective Effect ◽  
Hypoxia Inducible Factor ◽  
Protozoan Parasite ◽  
Artery Occlusion ◽  
Control Group ◽  
Triphenyltetrazolium Chloride ◽  
Neuroprotective Effects ◽  
Neurobehavioral Function

Toxoplasma gondii is an obligate intracellular protozoan parasite that can invade various organs in the host body, including the central nervous system. Chronic intracranial T. gondii is known to be associated with neuroprotection against neurodegenerative diseases through interaction with host brain cells in various ways. The present study investigated the neuroprotective effects of chronic T. gondii infection in mice with cerebral ischemia experimentally produced by middle cerebral artery occlusion (MCAO) surgery. The neurobehavioral effects of cerebral ischemia were assessed by measurement of Garcia score and Rotarod behavior tests. The volume of brain ischemia was measured by triphenyltetrazolium chloride staining. The expression levels of related genes and proteins were determined. After cerebral ischemia, corrected infarction volume was significantly reduced in T. gondii infected mice, and their neurobehavioral function was significantly better than that of the uninfection control group. Chronic T. gondii infection induced the expression of hypoxia-inducible factor 1-alpha (HIF-1α) in the brain before MCAO. T. gondii infection also increased the expression of vascular endothelial growth factor after the cerebral ischemia. It is suggested that chronic intracerebral infection of T. gondii may be a potential preconditioning strategy to reduce neural deficits associated with cerebral ischemia and induce brain ischemic tolerance through the regulation of HIF-1α expression.

scholarly journals Neuroprotective Effect of Physical Exercise on Neuronal Apoptosis Induced by Tramadol in Cerebral Cortex of Rats

2020 ◽  
Vol 10 (6) ◽  
pp. 7209-7222
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Physical Exercise ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Neuroprotective Effect ◽  
Physiological Saline ◽  
Male Rats ◽  
Control Group ◽  
Oxidative Stress Biomarkers

Tramadol is a centrally acting analgesic agent with low affinity for opioid receptors, used for treating moderate to severe pain. Tramadol, like other opioids, induces neuronal apoptosis, which causes multiple neuronal impairments. The current study was conducted to evaluate the potential neuroprotective role of physical exercises on tramadol-induced neuronal apoptosis in the cerebral cortex of rats. Thirty adult male rats were divided into three groups (n= 10) as follow; the control group was gavaged with physiological saline (0.9% NaCl); tramadol group was daily administered with tramadol (40 mg/kg) for 28 days, and physical exercise group was administered with the same dose as tramadol group, then rats were forced to run on the treadmill for 30 min, once a day for 28 days. Tramadol induced histopathological changes in the form of neuroses degeneration and apoptosis. These findings were confirmed by immunohistochemical and blotting studies, which showed upregulation of p53 and downregulation of Bcl-2. In addition, malondialdehyde (MDA), myeloperoxidase (MPO), and nuclear factor kappa B (NF-κB) significantly increased following tramadol administration. At the same time, glutathione (GSH) and glutathione peroxidase (GPx) were decreased. In contrast, physical exercise was found to protect cortical neurons from degeneration and apoptosis produced by tramadol. This was evidenced by the downregulation of p53 and upregulating Bcl-2 expression and the improved changes in the oxidative stress biomarkers in rats. Physical exercise reduced the neuronal apoptosis and degeneration in the cerebral cortex following tramadol administration through suppressing oxidative stress.

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