In Vitro Neuroprotective Effects of Macrophage Membrane-Derived Curcumin-Loaded Carriers against 1-Methyl-4-phenylpyridinium-Induced Neuronal Damage

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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Bilberry and its main constituents have neuroprotective effects against retinal neuronal damage in vitro and in vivo

Molecular Nutrition & Food Research ◽

10.1002/mnfr.200800394 ◽

2009 ◽

Vol 53 (7) ◽

pp. 869-877 ◽

Cited By ~ 61

Author(s):

Nozomu Matsunaga ◽

Shunsuke Imai ◽

Yuta Inokuchi ◽

Masamitsu Shimazawa ◽

Shigeru Yokota ◽

...

Keyword(s):

Neuronal Damage ◽

Neuroprotective Effects

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Integrated Proteomics and Lipidomics Investigation of the Mechanism Underlying the Neuroprotective Effect of N-benzylhexadecanamide

Molecules ◽

10.3390/molecules23112929 ◽

2018 ◽

Vol 23 (11) ◽

pp. 2929 ◽

Cited By ~ 1

Author(s):

Yanyan Zhou ◽

Hongjie Wang ◽

Feifei Guo ◽

Nan Si ◽

Adelheid Brantner ◽

...

Keyword(s):

Neurodegenerative Diseases ◽

Neuronal Damage ◽

Cell Model ◽

Neuroprotective Effect ◽

Interaction Network ◽

Sphingolipid Metabolism ◽

Neuronal System ◽

Neuroprotective Effects ◽

Lepidium Meyenii

Macamides are very important secondary metabolites produced by Lepidium meyenii Walp, which possess multiple bioactivities, especially in the neuronal system. In a previous study, we observed that macamides exhibited excellent effects in the recovery of injured nerves after 1-methyl-4-phenylpyridinium (MPP+)-induced dopaminergic neuronal damage in zebrafish. However, the mechanism underlying this effect remains unclear. In the present study, we observed that N-benzylhexadecanamide (XA), which is a typical constituent of macamides, improved the survival rate of neurons in vitro. We determined the concentration of neurotransmitters in MN9D cells and used it in conjunction with an integrated proteomics and lipidomics approach to investigate the mechanism underlying the neuroprotective effects of XA in an MPP+-induced neurodegeneration cell model using QqQ MS, Q-TOF MS, and Orbitrap MS. The statistical analysis of the results led to the identification of differentially-expressed biomarkers, including 11 proteins and 22 lipids, which may be responsible for the neuron-related activities of XA. All these potential biomarkers were closely related to the pathogenesis of neurodegenerative diseases, and their levels approached those in the normal group after treatment with XA. Furthermore, seven lipids, including five phosphatidylcholines, one lysophosphatidylcholine, and one phosphatidylethanolamine, were verified by a relative quantitative approach. Moreover, four proteins (Scarb2, Csnk2a2, Vti1b, and Bnip2) were validated by ELISA. The neurotransmitters taurine and norepinephrine, and the cholinergic constituents, correlated closely with the neuroprotective effects of XA. Finally, the protein–lipid interaction network was analyzed. Based on our results, the regulation of sphingolipid metabolism and mitochondrial function were determined to be the main mechanisms underlying the neuroprotective effect of XA. The present study should help us to better understand the multiple effects of macamides and their use in neurodegenerative diseases.

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Niosomes of Ascorbic Acid and α-Tocopherol in the Cerebral Ischemia-Reperfusion Model in Male Rats

BioMed Research International ◽

10.1155/2014/816103 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 11

Author(s):

Jaleh Varshosaz ◽

Somayeh Taymouri ◽

Abbas Pardakhty ◽

Majid Asadi-Shekaari ◽

Abodolreza Babaee

Keyword(s):

Ascorbic Acid ◽

Cerebral Ischemia ◽

Neuronal Damage ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Male Rats ◽

Size Change ◽

Neuroprotective Effects

The objective of the present study was to prepare a stableivinjectable formulation of ascorbic acid and α-tocopherol in preventing the cerebral ischemia. Different niosomal formulations were prepared by Span and Tween mixed with cholesterol. The physicochemical characteristics of niosomal formulations were evaluatedin vitro. Forin vivoevaluation, the rats were made ischemic by middle cerebral artery occlusion model for 30 min and the selected formulation was used for determining its neuroprotective effect against cerebral ischemia. Neuronal damage was evaluated by optical microscopy and transmission electron microscopy. The encapsulation efficiency of ascorbic acid was increased to more than 84% by remote loading method. The cholesterol content of the niosomes, the hydrophilicity potential of the encapsulated compounds, and the preparation method of niosomes were the main factors affecting the mean volume diameter of the prepared vesicles. High physical stability of the niosomes prepared from Span 40 and Span 60 was demonstrated due to negligible size change of vesicles during 6 months storage at 4–8°C.In vivostudies showed that ST60/Chol 35 : 35 : 30 niosomes had more neuroprotective effects against cerebral ischemic injuries in male rats than free ascorbic acid.

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Agmatine Alleviates Epileptic Seizures and Hippocampal Neuronal Damage by Inhibiting Gasdermin D-Mediated Pyroptosis

Frontiers in Pharmacology ◽

10.3389/fphar.2021.627557 ◽

2021 ◽

Vol 12 ◽

Author(s):

Xueying Li ◽

Jiahe Lin ◽

Yingjie Hua ◽

Jiaoni Gong ◽

Siqi Ding ◽

...

Keyword(s):

Nlrp3 Inflammasome ◽

Neuronal Damage ◽

Epileptic Seizures ◽

Inhibitory Effect ◽

Enzyme Linked Immunosorbent Assay ◽

Nissl Staining ◽

Neuroprotective Effects ◽

Cellular Inflammation

Background: Epilepsy is a common neurological disease, and neuroinflammation is one of the main contributors to epileptogenesis. Pyroptosis is a type of pro-inflammatory cell death that is related to epilepsy. Agmatine, has anti-inflammatory properties and exerts neuroprotective effects against seizures. Our study investigated the effect of agmatine on the core pyroptosis protein GSDMD in the context of epilepsy.Methods: A chronic epilepsy model and BV2 microglial cellular inflammation model were established by pentylenetetrazole (PTZ)-induced kindling or lipopolysaccharide (LPS) stimulation. H&E and Nissl staining were used to evaluate hippocampal neuronal damage. The expression of pyroptosis and inflammasome factors was examined by western blotting, quantitative real-time PCR, immunofluorescence and enzyme-linked immunosorbent assay (ELISA).Results: Agmatine disrupted the kindling acquisition process, which decreased seizure scores and the incidence of full kindling and blocked hippocampal neuronal damage. In addition, agmatine increased BV2 microglial cell survival in vitro and alleviated seizures in vivo by suppressing the levels of PTZ-induced pyroptosis. Finally, the expression of TLR4, MYD88, phospho-IκBα, phospho-NF-κB and the NLRP3 inflammasome was significantly upregulated in LPS-induced BV2 microglial cells, while agmatine suppressed the expression of these proteins.Conclusions: Our results indicate that agmatine affects epileptogenesis and exerts neuroprotective effects by inhibiting neuroinflammation, GSDMD activation, and pyroptosis. The inhibitory effect of agmatine on pyroptosis was mediated by the suppression of the TLR4/MYD88/NF-κB/NLRP3 inflammasome pathway. Therefore, agmatine may be a potential treatment option for epilepsy.

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Controlled Release of Ursodeoxycholic Acid from Pullulan Acetate Nanoparticles to Modulate Glutamate-Induced Excitotoxicity in PC-12 Cells

Journal of Nanomaterials ◽

10.1155/2018/7130450 ◽

2018 ◽

Vol 2018 ◽

pp. 1-12 ◽

Cited By ~ 1

Author(s):

Kwang Sik Yu ◽

Jun Young Oh ◽

Min Cheol Kim ◽

Seong Hee Kang ◽

Nam Seob Lee ◽

...

Keyword(s):

Ursodeoxycholic Acid ◽

Neuronal Damage ◽

Annexin V ◽

In Vitro Study ◽

Poly Vinyl Alcohol ◽

Neuroprotective Effects ◽

Transmission Electron ◽

Pullulan Acetate ◽

Related Proteins

The neuroprotective effects of the ursodeoxycholic acid- (UDCA-) loaded pullulan acetate (PA) (UDCA-PA) nanospheres stabilized by poly(vinyl alcohol) (PVA) were identified by in vitro study. The UDCA-PA nanospheres were constructed by nanoemulsion process. The UDCA-PA nanospheres were analyzed using Fourier transform-infrared spectroscopy (FT-IR) and transmission electron microscopy (TEM). Then, the UDCA-PA nanospheres were used to treat PC-12 neuronal cells, which were formerly triggered by glutamate-induced excitotoxicity. As a result, the cells treated with the UDCA-PA nanospheres showed higher survival rate against glutamate-induced excitotoxicity. Furthermore, the UDCA-PA nanospheres decreased immunoreactivity of Annexin V, a membrane marker for apoptotic cells, in PC-12 with glutamate-induced injury. Particularly, the UDCA-PA nanospheres decreased the level of apoptosis-related proteins such as caspase-3. Taken together, the UDCA-PA nanospheres increased neuroprotective effects against glutamate-induced neuronal damage via inhibition of apoptosis at low concentration.

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Propofol Exerts Greater Neuroprotection with Disodium Edetate than without It

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/sj.jcbfm.9600532 ◽

2007 ◽

Vol 28 (2) ◽

pp. 354-366 ◽

Cited By ~ 12

Author(s):

Yoshinori Kotani ◽

Yoshimi Nakajima ◽

Tatsuya Hasegawa ◽

Masahiko Satoh ◽

Hisamitsu Nagase ◽

...

Keyword(s):

Neuronal Damage ◽

Cell Damage ◽

Infarct Volume ◽

Zinc Homeostasis ◽

Terminal Deoxynucleotidyl Transferase ◽

Causal Mechanism ◽

Neuroprotective Effects ◽

Disodium Edetate

The main objective of this study, on mice, was to compare the neuroprotective effects of propofol with those of propofol plus disodium edetate (propofol EDTA). We also administered propofol EDTA (0.005% (w/v) EDTA) to mice intravenously, and measured the changes in zinc concentrations occurring after permanent middle cerebral artery occlusion. In the in vivo study, propofol EDTA displayed stronger neuroprotective effects than propofol alone. Furthermore, we examined the neuroprotective effects of EDTA administered alone, and found that EDTA Na significantly reduced the infarct volume. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling-positive cells in the ischemic penumbra was reduced more by propofol EDTA than by propofol alone. We performed in the in vitro study in five groups (aerobic, vehicle (control), propofol, EDTA, and propofol plus EDTA). Propofol and EDTA each protected PC12 cells against oxygen—glucose deprivation-induced cell damage, and the effect of propofol was increased by adding EDTA. Because the chelating action of EDTA was a potential causal mechanism, we examined the effect of propofol EDTA on intracerebral zinc homeostasis. When propofol EDTA was given intravenously 10 mins before cerebral ischemia, the zinc concentration decreased significantly in the cortical area, but not in the subcortex. In conclusion, (a) propofol provides neuroprotection against both in vivo and in vitro ischemic damage, and its effects are enhanced when EDTA is added; and (b) EDTA itself protects against ischemic neuronal damage, possibly, owing to its zinc-chelating action.

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Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Cellular Physiology and Biochemistry ◽

10.1159/000486768 ◽

2018 ◽

Vol 45 (1) ◽

pp. 212-225 ◽

Cited By ~ 9

Author(s):

Yunbo Shi ◽

Wang Miao ◽

Junfang Teng ◽

Lingli Zhang

Keyword(s):

Neuronal Apoptosis ◽

Neuronal Damage ◽

Dependent Manner ◽

Ginsenoside Rb1 ◽

Seizure Duration ◽

Neuroprotective Effects ◽

Induced Neuron ◽

Neuron Injury

Background/Aims: Ginsenoside Rb1 (Rb1) has been reported to have varieties of neuroprotective effects. This study aimed to evaluate the effects of Rb1 on pentylenetetrazol (PTZ)-induced rat brain injury and Mg2+ free-induced neuron injury and analyzed the detailed molecular mechanisms in vivo and in vitro. Methods: Seizure duration and latency were measured in epilepsy kindled rat. The cognitive impairment was assessed by Morris water maze (MWM) test. Oxidative stress parameters, malondialdehyde (MDA) and glutathione (GSH) were measured by the 2-thiobarbituric acid methods and the DTNB-GSSG reductase recycling methods. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Neuronal apoptosis was measured by Annexin V-FITC and propidium iodide (PI) staining. Immunohistochemistry and immunofluorescence staining were performed to evaluate Nrf2 and HO-1 expressions. Expression of Nrf2, HO-1, Bcl-2, iNOS and LC3 were evaluated by western blot. Results: The PTZ-injured rats presented longer seizure duration and shorter seizure latency. Rb1 ameliorated these effects, as well as the cognitive deficits caused by PTZ exposure. Besides, Rb1 dose-dependently increased GSH levels, decreased MDA levels and alleviated neuronal damage in PTZ-treated rats. In vitro, Rb1 increased cell viability and decreased neuronal apoptosis in a dose-dependent manner under Mg2+ free condition. Moreover, in vivo and in vitro, Rb1 enhanced both the Nrf2 and HO-1 expressions. Furthermore, upregulation of the expression of Bcl-2 and downregulation of the expression of iNOS and LC3 were observed. However, knockdown of Nrf2 adversely affected the protective effects of Rb1 in epileptic hippocampal neurons. Conclusion: Rb1 conferred neuroprotective effects against PTZ-induced brain damage and Mg2+ free-induced neuron injury by activating Nrf2/ARE signaling.

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Correlation of CGS 19755 Neuroprotection against in vitro Excitotoxicity and Focal Cerebral Ischemia

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1995.108 ◽

1995 ◽

Vol 15 (5) ◽

pp. 865-876 ◽

Cited By ~ 23

Author(s):

Miguel A. Pérez-Pinzón ◽

Carolina M. Maier ◽

Edward J. Yoon ◽

Guo-Hua Sun ◽

Rona G. Giffard ◽

...

Keyword(s):

Neuronal Damage ◽

Focal Cerebral Ischemia ◽

Neuroprotective Effect ◽

Primary Cultures ◽

Arterial Occlusion ◽

Neuroprotective Effects ◽

Brain Levels ◽

Cgs 19755

The in vivo neuroprotective effect and brain levels of cis-4-phosphonomethyl-2-piperidine carboxylic acid (CGS 19755), a competitive N-methyl-D-aspartate (NMDA) antagonist, were compared with its in vitro neuroprotective effects. The dose-response for in vitro neuroprotection against both NMDA toxicity and combined oxygen-glucose deprivation (OGD) was determined in murine neocortical cultures. Primary cultures of neocortical cells from fetal mice were injured by exposure to 500 μM NMDA for 10 min or to OGD for 45 min. The effect of CGS 19755 in both injury paradigms was assessed morphologically and quantitated by determination of lactate dehydrogenase release. Near complete neuroprotection was found at high doses of CGS 19755. The ED50 for protection against NMDA toxicity was 25.4 μmM, and against OGD the ED50 was 15.2 μM. For the in vivo paradigm rabbits underwent 2 h of left internal carotid, anterior cerebral, and middle cerebral artery occlusion followed by 4 h reperfusion; ischemic injury was assessed by magnetic resonance imaging and histopathology. The rabbits were treated with 40 mg/kg i.v. CGS 19755 or saline 10 min after arterial occlusion. CSF and brain levels of CGS 19755 were 12 μM and 5 μM, respectively, at 1 h, 6 μM and 5 μM at 2 h, and 13 μM and 7 μM at 4 h. These levels were neuroprotective in this model, reducing cortical ischemic edema by 48% and ischemic neuronal damage by 76%. These results suggest that a single i.v. dose penetrates the blood-brain barrier, attaining sustained neuroprotective levels that are in the range for in vitro neuroprotection.

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Appraisal of in vitro neuroprotective effects of Turkish Pinus L. species and pycnogenol and essential oil analyses

Planta Medica ◽

10.1055/s-0031-1282928 ◽

2011 ◽

Vol 77 (12) ◽

Author(s):

O Ustun ◽

F Senol ◽

M Kürkçüoğlu ◽

I Orhan ◽

M Kartal ◽

...

Keyword(s):

Essential Oil ◽

Neuroprotective Effects

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