Neuroprotective effects of phloretin and phloridzin on paclitaxel-induced neuronal damage in primary neuron cells

Gynura procumbens has been used in Southeast Asia for the treatment of hypertension, hyperglycemia, and skin problems induced by ultraviolet irradiation. Although considerable studies have reported the biological properties of Gynura procumbens root extract (GPE-R), there are no studies on the effects of GPE-R in brain damages, for example following brain ischemia. In the present study, we screened the neuroprotective effects of GPE-R against ischemic damage and neuroinflammation in the hippocampus based on behavioral, morphological, and biological approaches. Gerbils received oral administration of GPE-R (30 and 300 mg/kg) every day for three weeks and 2 h after the last administration, ischemic surgery was done by occlusion of both common carotid arteries for 5 min. Administration of 300 mg/kg GPE-R significantly reduced ischemia-induced locomotor hyperactivity 1 day after ischemia. Significantly more NeuN-positive neurons were observed in the hippocampal CA1 regions of 300 mg/kg GPE-R-treated animals compared to those in the vehicle-treated group 4 days after ischemia. Administration of GPE-R significantly reduced levels of pro-inflammatory cytokines such as interleukin-1β, -6, and tumor necrosis factor-α 6 h after ischemia/reperfusion. In addition, activated microglia were significantly decreased in the 300 mg/kg GPE-R-treated group four days after ischemia/reperfusion compared to the vehicle-treated group. These results suggest that GPE-R may be one of the possible agents to protect neurons from ischemic damage by reducing inflammatory responses.

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PRAMIPEXOLE DIHYDROCHLORIDE LOADED MPEGPCL NANOSUSPENSION BY MODIFIED NANOPRECIPITATION: IN VITRO AND IN VIVO EVALUATION

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2016.v9i6.13979 ◽

2016 ◽

Vol 9 (6) ◽

pp. 161

Author(s):

Soma Sundaram

Keyword(s):

Particle Size ◽

Zeta Potential ◽

Cell Viability ◽

Neuronal Damage ◽

Antioxidant Potential ◽

Enzymatic Antioxidants ◽

In Vivo Evaluation ◽

Neuroprotective Effects ◽

Pramipexole Dihydrochloride

AbstractAim and Objectives The present study was carried out to show the potential neuroprotective effects in both invitro and invivo pramipexole dihydrochloride nanosuspension for the treatment in Parkinson’s disease.Materials and Methods: Nanosuspension of pramipexole dihydrochloride was prepared with MPEG-PCL and Pluronic F68 by the process of modified nanoprecipitation technique with different concentrations of MPEG-PCL. The particle size, zeta potential, SEM, TEM and invitro dug release where performed. The cell viability study was performed by using SH-SY5Y cells. Further the formulation is evaluated for its antioxidant potential against rotenone induced neuronal damage in Wister rats such as enzymatic, non enzymatic antioxidants and histopathological evaluation.Result and Discussion: The nanoformulation shows least particle size of 143 nm and maximum zeta potential value 33.4 mv with 88.53% entrapment efficiency were observed with PMPNP 2 formulation. The SEM, TEM and invitro dug release of PMPNP 2 were shows spherical shape with controlled release when compared to other formulations. Further the MTT assay were performed by using SH-SY5Y cells which shows more than 50 % cell viability with 50 µl of PPMNP 2 nanoformulation. Further the antioxidant potential done in rotenone induced neuronal damage in Wister rats. The results showed elevation in the levels of enzymatic and non enzymatic antioxidants compared with neuronal toxic group. Further nanoformulation group showed decrease in levels of LPO which correlates with histopathological architecture.Conclusion: Our study concluded that nanoformulation showed better protective potential in both invitro and invivo compare to free drug for the treatment in Parkinson’s disease.Keywords: Pramipexoledihydrochloride; MPEG-PCL; SH-SY5Y cells; Nanoprecipitation; Parkinson’s disease.

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Neuroprotective Effects of IGF-I against TNFα-Induced Neuronal Damage in HIV-Associated Dementia

Virology ◽

10.1006/viro.2002.1690 ◽

2003 ◽

Vol 305 (1) ◽

pp. 66-76 ◽

Cited By ~ 29

Author(s):

Jin Ying Wang ◽

Francesca Peruzzi ◽

Adam Lassak ◽

Luis Del Valle ◽

Sujahata Radhakrishnan ◽

...

Keyword(s):

Neuronal Damage ◽

Neuroprotective Effects ◽

Igf I

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Neuroprotection via AT2 receptor agonists in ischemic stroke

Clinical Science ◽

10.1042/cs20171549 ◽

2018 ◽

Vol 132 (10) ◽

pp. 1055-1067 ◽

Cited By ~ 10

Author(s):

Douglas M. Bennion ◽

U. Muscha Steckelings ◽

Colin Sumners

Keyword(s):

Ischemic Stroke ◽

Neuronal Damage ◽

Recombinant Tissue Plasminogen Activator ◽

Neurological Deficits ◽

At2 Receptor ◽

Neuroprotective Effects ◽

Receptor Agonists ◽

Stroke Epidemiology ◽

The Brain

Stroke is a devastating disease that afflicts millions of people each year worldwide. Ischemic stroke, which accounts for ~88% of cases, occurs when blood supply to the brain is decreased, often because of thromboembolism or atherosclerotic occlusion. This deprives the brain of oxygen and nutrients, causing immediate, irreversible necrosis within the core of the ischemic area, but more delayed and potentially reversible neuronal damage in the surrounding brain tissue, the penumbra. The only currently approved therapies for ischemic stroke, the thrombolytic agent recombinant tissue plasminogen activator (rtPA) and the endovascular clot retrieval/destruction processes, are aimed at restoring blood flow to the infarcted area, but are only available for a minority of patients and are not able in most cases to completely restore neurological deficits. Consequently, there remains a need for agents that will protect neurones against death following ischemic stroke. Here, we evaluate angiotensin II (Ang II) type 2 (AT2) receptor agonists as a possible therapeutic target for this disease. We first provide an overview of stroke epidemiology, pathophysiology, and currently approved therapies. We next review the large amount of preclinical evidence, accumulated over the past decade and a half, which indicates that AT2 receptor agonists exert significant neuroprotective effects in various animal models, and discuss the potential mechanisms involved. Finally, after discussing the challenges of delivering blood–brain barrier (BBB) impermeable AT2 receptor agonists to the infarcted areas of the brain, we summarize the evidence for and against the development of these agents as a promising therapeutic strategy for ischemic stroke.

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Neuroprotective effects of thymoquinone against MDMA-induced neurotoxicity

Research Journal of Pharmacy and Technology ◽

10.52711/0974-360x.2021.01033 ◽

2021 ◽

pp. 5945-5952

Author(s):

Mustafa NS. ◽

Mohamad N. ◽

Abu Bakar NH. ◽

Mohd Adnan LH. ◽

Jeharsae R. ◽

...

Keyword(s):

Memory Impairment ◽

Natural Compound ◽

Neuronal Damage ◽

Memory Performance ◽

Novel Object Recognition ◽

Psychoactive Substance ◽

Sprague Dawley ◽

Hippocampal Dentate Gyrus ◽

Object Recognition Test ◽

Neuroprotective Effects

MDMA (3, 4-methylenedioxymethamphetamine) is a psychoactive substance that is associated with neurotoxicity. MDMA exposure to human results in the degeneration of neuronal cells in the hippocampus. Hence, the purpose of this study was to examine the potential of a natural compound known as thymoquinone (TQ) to protect against neuronal damage and memory impairment in rats stimulated by MDMA. The administration of TQ into MDMA-induced neuronal damage rats was carried out in male Sprague Dawley via a 1-week treatment dividing into four groups (n=36, 7-9 per group). The studied groups involved with the treatments comprise i) Control (1 mL/kg saline), ii) MDMA (10 mg/kg MDMA), iii) MDMA+TQ (10 mg/kg MDMA + 40 mg/kg TQ) and iv) TQ control (40 mg/kg TQ). A novel object recognition test (NORT) was carried out to evaluate the memory performance of the rats, followed by a histopathological assessment of the hippocampal dentate gyrus. The histopathology analysis revealed a significant increase in numbers of positive cells by Fluoro-Jade C following the effect of MDMA on neuronal damage (MDMA induced group) compared to control (P<0.05). Next, the TQ treatments observed in MDMA+TQ exhibited a decline in positive cells from Fluoro-Jade C. The index of recognition memory was found to be increased in MDMA+TQ compared to the MDMA alone (P<0.05). This study suggests that the neuronal damage inflicted by MDMA in a rat model has the potential to be treated by TQ.

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Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury

Scientific Reports ◽

10.1038/srep07091 ◽

2014 ◽

Vol 4 (1) ◽

Cited By ~ 27

Author(s):

Xiao-Ya Gao ◽

Jian-Ou Huang ◽

Ya-Fang Hu ◽

Yong Gu ◽

Shu-Zhen Zhu ◽

...

Keyword(s):

Cortical Neurons ◽

Mild Hypothermia ◽

Neuronal Damage ◽

Combined Treatment ◽

Neuronal Injury ◽

Glucose Deprivation ◽

Oxygen Glucose Deprivation ◽

Single Treatment ◽

Neuroprotective Effects ◽

Apoptosis Pathway

Abstract Co-treatment of neuroprotective reagents may improve the therapeutic efficacy of hypothermia in protecting neurons during ischemic stroke. This study aimed to find promising drugs that enhance the neuroprotective effect of mild hypothermia (MH). 26 candidate drugs were selected based on different targets. Primary cultured cortical neurons were exposed to oxygen-glucose deprivation and reoxygenation (OGD/R) to induce neuronal damage, followed by either single treatment (a drug or MH) or a combination of a drug and MH. Results showed that, compared with single treatment, combination of MH with brain derived neurotrophic factor, glibenclamide, dizocilpine, human urinary kallidinogenase or neuroglobin displayed higher proportion of neuronal cell viability. The latter three drugs also caused less apoptosis rate in combined treatment. Furthermore, co-treatment of those three drugs and MH decreased the level of reactive oxygen species (ROS) and intracellular calcium accumulation, as well as stabilized mitochondrial membrane potential (MMP), indicating the combined neuroprotective effects are probably via inhibiting mitochondrial apoptosis pathway. Taken together, the study suggests that combined treatment with hypothermia and certain neuroprotective reagents provide a better protection against OGD/R-induced neuronal injury.

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The Neuroprotective Effects ofRatanasampilon Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2015/792342 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 3

Author(s):

Aiqin Zhu ◽

Zhou Wu ◽

Jie Meng ◽

Patrick L. McGeer ◽

Yi Zhu ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Dna Damage ◽

Molecular Mechanisms ◽

Neuronal Damage ◽

Mitogen Activated Protein Kinase ◽

Tibetan Medicine ◽

Dependent Manner ◽

Neuroprotective Effects ◽

Human Neuroblastoma ◽

Traditional Tibetan Medicine

We previously found thatRatanasampil(RNSP), a traditional Tibetan medicine, improves the cognitive function of mild-to-moderate AD patients living at high altitude, as well as learning and memory in an AD mouse model (Tg2576); however, mechanism underlying the effects of RNSP is unknown. In the present study, we investigated the effects and molecular mechanisms of RNSP on oxidative stress-induced neuronal toxicity using human neuroblastoma SH-SY5Y cells. Pretreatment with RNSP significantly ameliorated the hydrogen peroxide- (H2O2-) induced cytotoxicity of SH-SY5Y cells in a dose-dependent manner (up to 60 μg/mL). Furthermore, RNSP significantly reduced the H2O2-induced upregulation of 8-oxo-2′-deoxyguanosine (8-oxo-dG, the oxidative DNA damage marker) but significantly reversed the expression of repressor element-1 silencing transcription factor (REST) from H2O2associated (100 μM) downregulation. Moreover, RNSP significantly attenuated the H2O2-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 (ERK 1/2) in SH-SY5Y cells. These observations strongly suggest that RNSP may protect the oxidative stress-induced neuronal damage that occurs through the properties of various antioxidants and inhibit the activation of MAPKs. We thus provide the principle molecular mechanisms of the effects of RNSP and indicate its role in the prevention and clinical management of AD.

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Neuroprotective Effects of PEP-1-Cu,Zn-SOD against Ischemic Neuronal Damage in the Rabbit Spinal Cord

Neurochemical Research ◽

10.1007/s11064-011-0613-0 ◽

2011 ◽

Vol 37 (2) ◽

pp. 307-313 ◽

Cited By ~ 21

Author(s):

Woosuk Kim ◽

Dae Won Kim ◽

Dae Young Yoo ◽

Jin Young Chung ◽

In Koo Hwang ◽

...

Keyword(s):

Spinal Cord ◽

Neuronal Damage ◽

Neuroprotective Effects

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Neuroprotective effects of adenosine deaminase in the striatum

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x15625077 ◽

2016 ◽

Vol 36 (4) ◽

pp. 709-720 ◽

Cited By ~ 7

Author(s):

Risa Tamura ◽

Hiroyuki Ohta ◽

Yasushi Satoh ◽

Shigeaki Nonoyama ◽

Yasuhiro Nishida ◽

...

Keyword(s):

Cerebral Ischemia ◽

Adenosine Deaminase ◽

Neuronal Damage ◽

Brain Slices ◽

Field Potential ◽

Glucose Deprivation ◽

Oxygen Glucose Deprivation ◽

Protective Effects ◽

Neuroprotective Effects ◽

Negative Effect

Adenosine deaminase (ADA) is a ubiquitous enzyme that catabolizes adenosine and deoxyadenosine. During cerebral ischemia, extracellular adenosine levels increase acutely and adenosine deaminase catabolizes the increased levels of adenosine. Since adenosine is a known neuroprotective agent, adenosine deaminase was thought to have a negative effect during ischemia. In this study, however, we demonstrate that adenosine deaminase has substantial neuroprotective effects in the striatum, which is especially vulnerable during cerebral ischemia. We used temporary oxygen/glucose deprivation (OGD) to simulate ischemia in rat corticostriatal brain slices. We used field potentials as the primary measure of neuronal damage. For stable and efficient electrophysiological assessment, we used transgenic rats expressing channelrhodopsin-2, which depolarizes neurons in response to blue light. Time courses of electrically evoked striatal field potential (eFP) and optogenetically evoked striatal field potential (optFP) were recorded during and after oxygen/glucose deprivation. The levels of both eFP and optFP decreased after 10 min of oxygen/glucose deprivation. Bath-application of 10 µg/ml adenosine deaminase during oxygen/glucose deprivation significantly attenuated the oxygen/glucose deprivation-induced reduction in levels of eFP and optFP. The number of injured cells decreased significantly, and western blot analysis indicated a significant decrease of autophagic signaling in the adenosine deaminase-treated oxygen/glucose deprivation slices. These results indicate that adenosine deaminase has protective effects in the striatum.

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Vitamin D and 17β-estradiol upregulate each other's receptors and regulating the AMPK/NF-κB pathway to relieve depressive-like behaviors in female ovariectomized rats

10.21203/rs.2.17057/v1 ◽

2019 ◽

Author(s):

Wen-yuan Zhang ◽

Yujin Guo ◽

Ke-yi Wang ◽

Pei Jiang

Keyword(s):

Vitamin D ◽

Neuronal Damage ◽

Chronic Administration ◽

Ovariectomized Rats ◽

Neuroprotective Effects ◽

Ovx Rats ◽

Increased Risk ◽

17Β Estradiol ◽

Induced Apoptosis ◽

Control Sham

Abstract Background: A deficiency of vitamin D (VD) or 17β-estradiol (E2) is associated with increased risk of mood disorders such as depression in menopausal females, but the mechanism underlying is still elusive. The present study aims to evaluate whether vitamin D and 17β-estradiol could relieve a depressive-like state through neuroinflammatory regulation in ovariectomized (OVX) rats. Methods: Female SD rats were randomly divided into four groups, namely, control (SHAM), OVX, OVX+VD, and OVX+E2. The treatment procedure was performed for 10 weeks until sacrifice. Results: The chronic administration of vitamin D and 17β-estradiol showed anti-depressive-like activity in the OVX rats. Additionally, vitamin D and 17β-estradiol upregulated each other's receptors, including VDR, ERα, and ERβ in the hippocampus of OVX rats. Vitamin D and 17β-estradiol showed neuroprotective effects by decreasing OVX-induced apoptosis and neuronal damage, regulating the AMPK/NF-κB signaling pathway, and reducing the proinflammatory cytokines (IL-1β, IL-6, and TNFα), as well as iNOS and COX-2 in the hippocampus of OVX rats. Conclusions: The present study demonstrated that vitamin D and 17β-estradiol could upregulate each other's receptors and regulate the AMPK/NF-κB pathway to relieve the OVX-induced depressive-like state. The results should stimulate translational research towards the vitamin D potential for prevention or treatment of menopause-related depression.

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