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.

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 Alleviation of Memory Deficit by Bergenin via the Regulation of Reelin and Nrf-2/NF-κB Pathway in Transgenic Mouse Model

2021 ◽  
Vol 22 (12) ◽  
pp. 6603
Author(s):  
Bushra Shal ◽  
Adnan Khan ◽  
Ashraf Ullah Khan ◽  
Rahim Ullah ◽  
Gowhar Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Neuroprotective Effect ◽  
Annexin V ◽  
Memory Deficit ◽  
Y Maze ◽  
Spatial Memory Deficit ◽  
Aβ Aggregation ◽  
Ft Ir ◽  
Reelin Signaling

The present study aims to determine the neuroprotective effect of Bergenin against spatial memory deficit associated with neurodegeneration. Preliminarily, the protective effect of Bergenin was observed against H2O2-induced oxidative stress in HT-22 and PC-12 cells. Further studies were performed in 5xFAD Tg mouse model by administering Bergenin (1, 30 and 60 mg/kg; orally), whereas Bergenin (60 mg/kg) significantly attenuated the memory deficit observed in the Y-maze and Morris water maze (MWM) test. Fourier transform-infrared (FT-IR) spectroscopy displayed restoration of lipids, proteins and their derivatives compared to the 5xFAD Tg mice group. The differential scanning calorimeter (DSC) suggested an absence of amyloid beta (Aβ) aggregation in Bergenin-treated mice. The immunohistochemistry (IHC) analysis suggested the neuroprotective effect of Bergenin by increasing Reelin signaling (Reelin/Dab-1) and attenuated Aβ (1–42) aggregation in hippocampal regions of mouse brains. Furthermore, IHC and western blot results suggested antioxidant (Keap-1/Nrf-2/HO-1), anti-inflammatory (TLR-4/NF-kB) and anti-apoptotic (Bcl-2/Bax/Caspase-3) effect of Bergenin. Moreover, a decrease in Annexin V/PI-stained hippocampal cells suggested its effect against neurodegeneration. The histopathological changes were reversed significantly by Bergenin. In addition, a remarkable increase in antioxidant level with suppression of pro-inflammatory cytokines, oxidative stress and nitric oxide production were observed in specific regions of the mouse brains.

N-Myc Downstream-Regulated Gene 2 (Ndrg2): A Critical Mediator of Estrogen-Induced Neuroprotection Against Cerebral Ischemic Injury

2021 ◽  
Author(s):  
Lixia Zhang ◽  
Yulong Ma ◽  
Min Liu ◽  
Miao Sun ◽  
Jin Wang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Male Mice ◽  
Neuroprotective Effects ◽  
Female Mice ◽  
Ndrg2 Expression ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

Abstract Growing evidence indicates that estrogen plays a pivotal role in neuroprotection against cerebral ischemia, but the molecular mechanism of this protection is still elusive. N-myc downstream‐regulated gene 2 (Ndrg2), an estrogen-targeted gene, has been shown to exert neuroprotective effects against cerebral ischemia in male mice. However, the role of Ndrg2 in the neuroprotective effect of estrogen remains unknown. In this study, we first detected NDRG2 expression levels in the cortex and striatum in both female and male mice with western blot analyses. We then detected cerebral ischemic injury by constructing middle cerebral artery occlusion and reperfusion (MCAO-R) models in Ndrg2 knockout or conditional knockdown female mice. We further implemented estrogen, ERα or ERβ agonist replacement in the ovariectomized (OVX) Ndrg2 knockouts or conditional knockdowns female mice, then tested for NDRG2 expression, glial fibrillary acidic protein (GFAP) expression, and extent of cerebral ischemic injury. We found that NDRG2 expression was significantly higher in female than in male mice in both the cortex and striatum. Ndrg2 knockouts and conditional knockdowns showed significantly aggravated cerebral ischemic injury in female mice. Estrogen and ERβ replacement treatment (DPN) led to NDRG2 upregulation in both the cortex and striatum of OVX mice. Estrogen and DPN also led to GFAP upregulation in OVX mice. However, the effect of estrogen and DPN in activating astrocytes was lost in Ndrg2 knockouts OVX mice and primary cultured astrocytes, but partially retained in conditional knockdowns OVX mice. Most importantly, we found that the neuroprotective effects of E2 and DPN against cerebral ischemic injury were lost in Ndrg2 knockouts OVX mice but partially retained in conditional knockdowns OVX mice. These findings demonstrate that estrogen alleviated cerebral ischemic injury via ERβ upregulation of Ndrg2, which could activate astrocytes, indicating that Ndrg2 is a critical mediator of E2-induced neuroprotection against cerebral ischemic injury.

scholarly journals Effect of Grinding and Subsequent Various Surface Treatments on the Surface Roughness of Full Contour Monolithic Zirconia

2021 ◽  
Vol 10 (32) ◽  
pp. 2624-2628
Author(s):  
Surya Teja ◽  
Sanath Kumar Shetty ◽  
Mohammed Mohammed ◽  
Karkala Syed ◽  
Uma Mayoor ◽  
...  
Keyword(s):  
Surface Roughness ◽  
Surface Treatments ◽  
Control Group ◽  
Dental Procedures ◽  
Significant Difference ◽  
Monolithic Zirconia ◽  
Spss Software ◽  
Natural Dentition ◽  
Post Hoc ◽  
Control Group Group

BACKGROUND A smooth zirconia surface is necessary to protect the opposing natural dentition, to prevent plaque accumulation and to increase the survival rate of restoration by reducing the chances of failure by crack propagation. Surface roughness can be incorporated by routine dental procedures done in labs and clinics to adjust the restoration. It is unclear which surface treatment is most appropriate to achieve clinically acceptable zirconia surface. The purpose of this study was to evaluate the effect of grinding and subsequent various surface treatments on the surface roughness of full contour monolithic zirconia. METHODS In this invitro study 10 zirconia bars of final dimensions 20 x 4 x 2 mm & 40 zirconia bars of final dimensions 20 x 4 x 2.2 mm were milled and sintered. The zirconia bars with final dimensions 20 x 4 x 2mm were glazed and selected as samples for control group (Group C) (n = 10). Forty zirconia bars with dimensions of 20 x 4 x 2.2 mm were grounded using a standard straight cylindrical diamond point (105 – 125 µm) by placing them in a customized grinding apparatus till the dimensions became similar to that of control group i.e. 20 x 4 x 2 mm. After grinding and confirming the dimensions of each full contour monolithic zirconia bar using digital vernier caliper, zirconia bars were randomly allocated into 4 groups with 10 samples in each group (n = 10), namely (Group G: Grinding only, Group G+R: Grinding & Reheating, Group G+G: Grinding & Glazing, Group G+P: Grinding & Polishing) respectively. Surface roughness values were measured using a profilometer. Differences between groups were examined using one-way analysis of variance (ANOVA) (P ≤ 0.05) and Post hoc Tukey HSD test was done for multiple comparisons of surface roughness in between the groups using Statistical Package for Social Sciences (SPSS) software. RESULTS Group C showed the least surface roughness values. The maximum surface roughness values were seen in Group G. Surface roughness of Group G, Group G + H and Group G + G were statistically significant from Group C and Group G + P. There was no statistically significant difference in surface roughness values between Group C and Group G + P. CONCLUSIONS It can be concluded that polishing after grinding significantly reduced the surface roughness and re-established the surface smoothness of full-contour monolithic zirconia bars. KEY WORDS Surface Roughness, Zirconia, Monolithic, Full Contour, Profilometer

scholarly journals Thymoquinone Improved Nonylphenol-Induced Memory Deficit and Neurotoxicity Through its Antioxidant and Neuroprotective Effects

2021 ◽  
Author(s):  
Mandana Lotfi ◽  
Sohrab Kazemi ◽  
Anahita Ebrahimpour ◽  
Fereshteh Pourabdolhossein ◽  
Leila Satarian ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Nigella Sativa ◽  
Neuroprotective Effect ◽  
In Vitro Study ◽  
Alpha Synuclein ◽  
Memory Deficit ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
Neuroprotective Effects

Abstract Nonylphenol (NP), a well-known endocrine-disrupter chemical, has several harmful effects on the central nervous system including neuroendocrine disruption, cognitive impairment, and neurotoxicity. Thymoquinone (TQ) is a main bioactive compound in the black seeds of Nigella sativa that has antioxidant, anti-inflammatory, and neuroprotective properties. Here, we investigated the neuroprotective effect of TQ against NP-induced memory deficit and neurotoxicity in rats. To induce memory impairment, NP (25 mg/kg) was used as gavage in male Wistar rats for 21 days. TQ (2.5, 5 and 10mg/kg) was intraperitoneally administered in NP-treated animals. The morris water maze test was performed to assess spatial learning and memory. The hippocampal tissues were isolated from the brain for histopathological evaluation. Biochemical, molecular and cellular tests were performed to quantify oxidant (malondialdehyde; MDA)/antioxidant (superoxide dismutase (SOD), total antioxidant capacity (TAC) and reduced glutathione (GSH) parameters as well as markers for astrocytic activation (glial fibrillary acidic protein; GFAP) and neuronal death (alpha-synuclein; α-syn). Results showed TQ (5 mg/kg) significantly improved NP-induced memory impairment. Histological data revealed a significant increase in the number of necrotic cells in hippocampus, and TQ treatment markedly decreased this effect. The GSH and TAC levels were significantly increased in TQ-treated groups compared to NP group. The molecular analysis indicated that NP increased GFAP and decreased α-syn expression and TQ treatment did the reverse. In vitro study in astrocytes isolated from mice brain showed that TQ significantly increased cell viability in NP-induced cytotoxicity. This study strongly indicates that TQ has neuroprotective effects on NP-induced neurotoxicity through reducing oxidative damages and neuroinflammation.

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.

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 Phenolic Compounds Isolated and Identified from Amla (Phyllanthus emblica) Juice Powder and their Antioxidant and Neuroprotective Activities

2018 ◽  
Vol 13 (10) ◽  
pp. 1934578X1801301 ◽  
Author(s):  
Kenneth Rose ◽  
Chunpeng Wan ◽  
Amber Thomas ◽  
Navindra P. Seeram ◽  
Hang Ma
Keyword(s):  
Gallic Acid ◽  
Ellagic Acid ◽  
Chemical Constituents ◽  
Butylated Hydroxytoluene ◽  
Neuroprotective Activity ◽  
Control Group ◽  
Phyllanthus Emblica ◽  
Neuroprotective Effects ◽  
Potential Health

The edible fruit of Phyllanthus emblica (known as amla and Indian gooseberry) is widely used in Eastern traditional medicinal systems for a variety of ailments. Our group has previously reported that an amla juice powder shows neuroprotective effects in several in vitro and in vivo assay models but its chemical constituents and their neuroprotective activity remain unknown. Therefore, we conducted a phytochemical investigation of amla juice powder and evaluated the antioxidant and neuroprotective effects of the isolates. Ten phenolics (1–10), including gallic acid (1), five gallic acid derivatives (2–6), ellagic acid (7), and three ellagic acid derivatives (8–10), were isolated and identified with compounds 8–10 being reported from amla for the first time. All of the isolates showed antioxidant effects in the DPPH assay with IC50 values ranging from 6-158.9 μM superior to the synthetic commercial antioxidant, butylated hydroxytoluene (IC50 = 371.4 μM). In addition, compound 8 reduced β-amyloid-induced neurotoxicity in a transgenic Caenorhabditis elegans model by increasing their survival rate by 28.3% compared to the control group. This study adds to the growing body of evidence supporting the potential health benefits of amla and supports the functional food and nutraceutical applications of amla juice powder.

scholarly journals Insulin and glucagon share the same mechanism of neuroprotection in diabetic rats: role of glutamate

2011 ◽  
Vol 301 (3) ◽  
pp. R668-R673 ◽  
Author(s):  
Rami Abu Fanne ◽  
Taher Nassar ◽  
Samuel N. Heyman ◽  
Nuha Hijazi ◽  
Abd Al-Roof Higazi
Keyword(s):  
Amino Acids ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Diabetic Rats ◽  
Metabolic Effects ◽  
Therapeutic Window ◽  
Neuroprotective Effects ◽  
Glucose Levels ◽  
Cerebral Artery Occlusion

In patients with acute ischemic stroke, diabetes and hyperglycemia are associated with increased infarct size, more profound neurologic deficits and higher mortality. Notwithstanding extensive clinical and experimental data, treatment of stroke-associated hyperglycemia with insulin is controversial. In addition to hyperglycemia, diabetes and even early prediabetic insulin resistance are associated with increased levels of amino acids, including the neurotoxic glutamate, in the circulation. The pleiotropic metabolic effects of insulin include a reduction in the concentration of amino acids in the circulation. In this article, we show that in diabetic rats exposed to transient middle cerebral artery occlusion, a decrease of plasma glutamate by insulin or glucagon reduces CSF glutamate, improves brain histology, and preserves neurologic function. The neuroprotective effect of insulin and glucagon was similar, notwithstanding their opposite effects on blood glucose. The therapeutic window of both hormones overlapped with the short duration (∼30 min) of elevated brain glutamate following brain trauma in rodents. Similar neuroprotective effects were found after administration of the glutamate scavenger oxaloacetate, which does not affect glucose metabolism. These data indicate that insulin and glucagon exert a neuroprotective effect within a very brief therapeutic window that correlates with their capacity to reduce glutamate, rather than by modifying glucose levels.

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.

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