scholarly journals Evaluation of Neuroprotective effect of medicinal plants in Drosophila melanogaster model

2018 ◽  
Vol 6 (03) ◽  
pp. 09-12
Author(s):  
Prakash Chaudhary ◽  
Swati Dhande
Keyword(s):  
Drosophila Melanogaster ◽  
Culture Medium ◽  
Neuroprotective Effect ◽  
Ethanolic Extract ◽  
Control Group ◽  
Therapeutic Approaches ◽  
Neuroprotective Effects ◽  
Negative Geotaxis ◽  
Locomotor Impairment ◽  
Locomotor Deficits

In this study, we investigated the neuroprotective effects of ethanolic extract of Bombax ceiba (EEBC) and ethanolic extract of Gymnemasylvestre (EEGS) against the toxicity induced by rotenone (ROT) in Drosophila melanogaster. Materials and Methods:Adult wild-type flies were concomitantly exposed to ROT (500 μM), EEBC (0.05% w/v and 0.1% w/v) and EEGS (0.05% w/v and 0.1% w/v) in the culture medium for 7 days. Results: ROT treated flies produced marked decreased in locomotor performance (i.e., climbing capability) in the negative geotaxis assay when compared to control group. EEBC and EEGS flies after treatment offered protection (24-42%) against the ROT-induced locomotor impairment in the negative geotaxis assay suggesting attenuation of ROT-induced locomotor deficits. Conclusion: The results of this study suggest that EEBC and EEGS were effective in reducing the toxicity induced by ROT in D. melanogaster as well as it confirms the significance of this model to explore possible therapeutic approaches in Parkinson’s disease (PD).

scholarly journals Neuroprotective Effect of Grewia carpinifolia Extract against Vanadium Induced Behavioural Impairment

2016 ◽  
Vol 60 (4) ◽  
pp. 5-13 ◽  
Author(s):  
O. E. Adebiyi ◽  
J. O. Olopade ◽  
F. O. Olayemi
Keyword(s):  
Neuroprotective Effect ◽  
Ethanolic Extract ◽  
Control Group ◽  
Protective Agent ◽  
Central Nervous System Toxicity ◽  
Sodium Metavanadate ◽  
Latent Time ◽  
Group A ◽  
Vanadium Toxicity ◽  
Group B

Abstract Vanadium (V), a heavy metal, has been reported to induce central nervous system toxicity leading to various behavioural impairments. It is characterized by the production of reactive oxygen. The present study was designed to test the possibility of Grewia carpinifolia ethanolic extract in preventing behavioural alterations following acute vanadium toxicity in mice. Twenty five Swiss albino mice (25—27 g) were completely randomized into 5 groups (A—E) of 5 animals each. Group A received distilled water and served as a control; group B, received vitamin E (500 mg.kg−1 b. w. every 72 hours), a known antioxidant orally, along with a daily dose of sodium metavanadate intraperitoneally (i. p.) for 7 days; group C and group D received Grewia carpinifolia leaf extract at 100 and 200 mg.kg−1 b.w orally respectively, along with the sodium metavanadate i. p. for 7 days; while group E received sodium metavanadate i. p. only for 7 days. The behavioural and motor functions were analysed by the open field, negative geotaxis, and hanging wire tests; the daily body and brain weights were recorded. Grewia carpinifolia ethanolic extracts significantly reduced the number of grooming, stretched attend posture, and freezing time that were significantly increased in the vanadium only group and also enhanced the vestibular functions. In addition, the latent time spent on the hanging wire in groups simultaneously administered with the extract and V compared favourably (P > 0.05) with the control groups but a decrease in latent time was observed in the V only group. The results suggest that acute V toxicity results in various behavioural deficits and support a possible role of Grewia carpinifolia as a protective agent against acute vanadium-toxicity with a better result at 200 mg.kg−1 b. w.

scholarly journals Traumatic injury in female Drosophila melanogaster affects the development and induces behavioral abnormalities in the offspring

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Ved Chauhan ◽  
Abha Chauhan
Keyword(s):  
Drosophila Melanogaster ◽  
Social Interaction ◽  
First Generation ◽  
Nearest Neighbor ◽  
Behavioral Assessment ◽  
Traumatic Injury ◽  
Well Being ◽  
Fruit Flies ◽  
Control Group ◽  
Negative Geotaxis

Abstract Traumatic injury (TI) during pregnancy increases the risk for developing neurological disorders in the infants. These disorders are a major concern for the well-being of children born after TI during pregnancy. TI during pregnancy may result in preterm labor and delivery, abruptio placentae, and/or fetomaternal hemorrhage. Drosophila melanogaster (fruit fly) is a widely used model to study brain and behavioral disorders in humans. In this study, we analyzed the effects of TI to female fruit flies on the development timing of larvae, social interaction and the behavior of offspring flies. TI to the female flies was found to affect the development of larvae and the behavior of offspring flies. There was a significant increase in the length of larvae delivered by traumatically injured maternal flies as compared to larvae from control maternal flies (without TI). The pupae formation from larvae, and the metamorphosis of pupae to the first generation of flies were faster in the TI group than the control group. Negative geotaxis and distance of the fly to its nearest neighbor are parameters of behavioral assessment in fruit flies. Negative geotaxis significantly decreased in the first generation of both male (p = 0.0021) and female (p = 0.0426) flies. The distance between the first generation of flies to its nearest neighbor was shorter in both male and female offspring flies in the TI group as compared to control group flies. These results indicate that TI to the female flies affected the development of larvae and resulted in early delivery, impaired social interaction and behavioral alterations in the offspring.

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 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>

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 Effects of Purple Sweet Potato Balinese Cultivar in Wistar Rats With Ischemic Stroke

2018 ◽  
Vol 6 (11) ◽  
pp. 1959-1964 ◽  
Author(s):  
I Made Oka Adnyana ◽  
AA Raka Sudewi ◽  
DPG Purwa Samatra ◽  
DN Suprapta
Keyword(s):  
Ischemic Stroke ◽  
Cytochrome C ◽  
Sweet Potato ◽  
Ipomoea Batatas ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Apoptosis Rate ◽  
Purple Sweet Potato

BACKGROUND: Purple sweet potato (Ipomoea Batatas L.) is one of the sources for anthocyanin, which promotes the health through antioxidant, anti-inflammatory, anti-cancer, neuroprotection, and anti-apoptosis activities. Oxidative stress has been shown to be the cause of apoptosis in ischemic stroke. AIM: The objective of this research was to delineate the pleiotropic effects of anthocyanin for neuroprotection during an acute stroke event. METHODS: Anthocyanin was extracted from Balinese cultivar of purple sweet potato and subsequently administered to rat models of induced ischemic stroke (labelled as treatment group), as well as a placebo (labelled as a control group). Several parameters were in turn evaluated, i.e. the activities of anti-apoptotic (Bcl-2) as well as pro-apoptotic (cytochrome c, caspase-3) molecules, and apoptosis rate. Bcl-2 levels were determined using the histochemical method, cytochrome c and caspase-3 via ELISA method, while apoptosis rate was measured by TdT-medicated Dutp-Nick End Labeling (TUNEL) assay. RESULTS: Bcl-2 expression demonstrated significantly higher Bcl-2 expression in the treatment compared with control group (median 31.2 vs. 1.1; p = 0.001). Accordingly, pro-apoptotic cytochrome c and caspase-3 levels were also found significantly lower in the treatment as opposed to control group (mean 4.17 vs. 8.06; p = 0.001; mean 3.81 vs. 8.02; p = 0.001). Ultimately, apoptosis rate was found markedly lower among treatment than control groups (mean 3.81 vs. control 21.97; p = 0.003). CONCLUSION: The results of this study indicated a significant neuroprotective effect of anthocyanin derived from Balinese cultivar of PSP. Anthocyanin was able to increase and reduce anti-apoptotic and pro-apoptotic protein levels, respectively, resulting in lesser cellular apoptotic rate when compared with placebo. The potential mechanism was thought mainly due to its anti-oxidant properties.

scholarly journals Evaluation of the protective effect of Paeonia emodi Wall on rat model of Parkinson’s disease induced by 6 hydroxy dopamine

2018 ◽  
Vol 7 (11) ◽  
pp. 2137
Author(s):  
Sharmila V. Jalgaonkar ◽  
Abhay P. Kamble ◽  
Urwashi I. Parmar ◽  
Dnyaneshwar G. Kurle ◽  
Moin S. Bedrekar ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuroprotective Effect ◽  
Protective Action ◽  
Ethanolic Extract ◽  
Neuroprotective Activity ◽  
Control Group ◽  
Biochemical Estimation ◽  
Dose Dependent ◽  
Muscular Coordination

Background: Generation of reactive oxygen species together with paucity of antioxidant defense is considered as an important cause for dopaminergic neuronal death. Review of literature indicates that none of the drugs so far studied for preventing the PD were found to be promising for use. Therefore, the present study was planned to evaluate the neuroprotective effect of Paeonia emodi Wall (PEW) in 6-hydroxy dopamine induced Parkinson’s disease (PD) model.Methods: The study was conducted on Wistar rats where Parkinson’s disease was induced by producing the striatal 6-hydroxy dopamine lesions. The test animals received ethanolic extract of PEW at dose of 200 and 300mg/kg for 28 days. Circling behavior, spontaneous locomotor activity, muscular coordination and akinesia were studied. Antioxidant levels were assessed by biochemical estimation and histopathology was carried out for dopaminergic neuronal loss.Results: PEW ethanolic extract showed significant dose dependent recovery in number of circlings, line crossing, muscular coordination and akinesia. A significant increase in MDA levels and decreased GSH level in PEW treated groups was observed in test groups as compared to control group (p<0.05). Normal architecture was retained only in PEW 300mg/Kg (p<0.05). L-Dopa did not showed effect on biochemical and histological parameters.Conclusions: The ethanolic extract of PEW showed neuroprotective activity against 6-hydroxy dopamine induced Parkinson’s disease in rats in both 200 and 300mg/kg doses. The protective action of PEW in PD can be because of its ability to reduce the oxidative stress.

Abstract TMP36: Exogenous Oxytocin Confers Significant Neuroprotective Effects and Improves Recovery in Young and Aged Animals After Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Juneyoung Lee ◽  
Yan Xu ◽  
Diego Morales Scheihing ◽  
Louise McCullough ◽  
Venugopal Reddy Venna
Keyword(s):  
Neuroprotective Effect ◽  
Control Group ◽  
Male Mice ◽  
Behavioral Recovery ◽  
Neuroprotective Effects ◽  
Delayed Treatment ◽  
Aged Mice ◽  
Beneficial Effects ◽  
Human Use ◽  
To Receive

Introduction: Oxytocin (OXT) is a highly evolutionary conserved neuropeptide and an important modulator of inflammation in response to stressors such as ischemia. Recent studies have implicated OXT signaling in neuroprotection in young mice after ischemic injury, but it is not known if OXT is efficacious in aged animals. In our ongoing studies, we found that OXT levels decline after stroke and with age. Therefore, we tested if exogenous OXT administration could provide beneficial effects and improve recovery in aged animals. Methods: Aged (18-20m) C57BL/6 male mice were purchased from Jax Labs and aged in house. Stroke was induced by a right MCAO-60min. Mice were randomly assigned to receive OXT or Atosiban, an OXT antagonist (OXTA) (0.5mg/kg) or vehicle. In the first set of experiments, aged mice were pre-treated with OXT, vehicle, or OXTA for 10 days before stroke. Infarcts were quantified 7-days after stroke (n=6-9/grp). In a second set, we tested the efficacy of delayed treatment, at 3hrs after stroke, and OXT was administered intranasally or i.p.. Functional and behavioral recovery and brain infarct size was assessed 7-day post-stroke. OXT levels 24hrs after stroke in human plasma were measured. Results: OXT treatment (0.5mg/kg/i.p. QD) prior to stroke led to significant neuroprotection in aged male mice, whereas OXTA treatment significantly increased infarct (p<0.05, n=6-9/grp) compared to control group (total: 39.4±2.9% control; 20.8±3.1% OXT; 51.3±2.8% OXTA). Importantly, no differences in cerebral blood flow or temperature were seen between groups. Interestingly, the neuroprotective effect of OXT treatment was observed even when treatment was initiated 3hrs (administered either i.p. or nasally) after stroke onset. Also, we observed a significant decrease in circulating OXT levels at 24hrs in stroke patients (n=26) compared to healthy controls, highlighting the translational relevance of this pathway. Conclusions: We found that OXT treatment either before or after stroke is neuroprotective in aged mice and both i.p. and nasal OXT administration improves recovery in parallel to reductions in brain injury. Given that intranasal formulations of OXT are approved for human use, our proposed strategy of supplementing OXT is highly translatable.

scholarly journals Neuroprotective Effect of Gallic Acid on Memory Deficit and Content of BDNF in Brain Entorhinal Cortex of Rat’s Offspring in Uteroplacental Insufficiency Model

2020 ◽  
Author(s):  
Zahra Esfandiari ◽  
Mohammad Amin Edalatmanesh
Keyword(s):  
Gallic Acid ◽  
Entorhinal Cortex ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Memory Deficit ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Y Maze ◽  
Spss Software ◽  
Post Hoc

Introduction: Uteroplacental insufficiency (UPI) causes neurodevelopmental deficits affecting the intrauterine growth restricted (IUGR) offspring. This study aimed to analyze the effects of Gallic acid (GA) on memory deficit and brain-derived neurotrophic factor (BDNF) content in entorhinal cortex of UPI rat models. Methods: In this experimental study, 40 pregnant Wistar rats were randomly divided into 5 groups, including: control, UPI, UPI+GA100, UPI+GA200and UPI+GA400. For IUGR induction, anterior uterine artery occlusion surgery was carried out on gestation day (GD) 18. From GD15, GA was administrated orally, in 100, 200 and 400 mg/kg BW doses until the birth of their neonates. Spatial and working memories are analyzed by Morris water maze and Y maze at postnatal day (PND) 30, respectively. Then, BDNF cerebral cortex level was estimated using ELISA technique.The data were analyzed through ANOVA and Tukey Post hoc in SPSS software version 16. Results: A significant decrease was observed in spatial and working memories and BDNF content in entorhinal cortex of UPI group in comparison with the control group (p˂0.05). On the other hand, GA-treated groups showed a significant increase in BDNF content and amelioration of spatial and working memories (p˂0.05). Conclusion: Fetal growth restrictionafter UPI by decreasingBDNFlevel in entorhinal cortex caused memory deficits in rat’s model. Moreover, neuroprotective effects of GA lead to increased BDNF content and ameliorate cognitive deficits in UPI model.

Sign in / Sign up

Export Citation Format

Share Document