scholarly journals Neuroprotective Effect of Filgrastim in Animal Models of 3-Nitropropionic Acid & Haloperidol Induced Neurotoxicity in Rats

2021 ◽  
Author(s):  
Vikrant Rahi ◽  
Parladh Ram ◽  
PUNEET KUMAR
Keyword(s):  
Animal Models ◽  
Movement Disorders ◽  
Motor Coordination ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Biochemical Alterations ◽  
Nitropropionic Acid ◽  
Pre Treatment ◽  
Haloperidol Treatment

Abstract Movement disorders are the heterogeneous group of disorders characterized by the progressive and selective impairment in motor function. Movement disorders like Huntington's disease (HD) and Tardive dyskinesia (TD) share many common features at both cellular and subcellular levels. Filgrastim is a recombinant methionyl granulocyte colony-stimulating factor (GCSF), shows neuroprotective properties in in-vivo models of movement disorders. The present study was designed to evaluate the neuroprotective effect of filgrastimin the animal models of haloperidol and 3-NP induced neurotoxicity in rats. Study was divided in two different protocol, in study one, rats were administered with haloperidol for 21 days, and filgrastim at the dose of (20, 40 & 60 µg/kg,s.c.) was administered once a day, before haloperidol treatment and the following parameters (orofacial movements, rotarod, actophotometer) were assessed for TD. Similarly, in second study rats were administered with 3-NP for 21 days and filgrastimat the dose of (20 & 40 µg/kg, s.c.) was administered, and following parameters (rotarod, narrow beam walk and open field test) were assessed for HD. In each study, on 22nd day, animals were sacrificed, to isolate cortex and striatum for oxidative stress (LPO, GSH, SOD, catalase, and nitrate) parameters. The result revealed that haloperidol and 3-NP treatment significantly impaired motor coordination, oxidative defense and induce TD and HD like symptoms. Filgrastim pre-treatment significantly averted haloperidol & 3-NP induced behavioral and biochemical alterations, respectively. Conclusively, neuroprotective effect of filgrastim is credited to its antioxidant properties, hence filgrastim might be a novel therapeutic candidate to manage TD & HD.

scholarly journals Neuroprotective effect of thiamine triethylorthoformate conjugate against Parkinson disease in a mouse model

2021 ◽  
Vol 18 (5) ◽  
pp. 1041-1047
Author(s):  
Yan Dong ◽  
Qing Xu ◽  
Xi Jia ◽  
Chao Li ◽  
Dan Xu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Parkinson Disease ◽  
Caspase 3 ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Down Regulation ◽  
Pre Treatment ◽  
Jnk Activation

Purpose: To investigate the effect of thiamine triethylorthoformate conjugate (TTO) on Parkinson disease (PD) in vitro and in vivo in a mice model. Methods: The effect of TTO on behavioural changes in PD mouse model was studied using pole, traction and swimming tests. Astrocyte proliferation after TTO treatment was assessed using 3 (4, 5 dimethyl 2 thi¬azolyl) 2, 5 diphenyl 2 H tetrazolium bromide (MTT) assay. Apoptosis was determined with flow cytometry using Annexin V Fluorescein isothiocyanate kit. Results: Treatment of PD mice with TTO led to a decrease in climbing time, increase in suspension score and enhancement of swimming score, when compared to the untreated group (p < 0.05). Treatment of astrocytes with TTO prior to MPP incubation significantly increased proliferation (p < 0.05). Apoptosis induction in astrocytes by MPP was attenuated by pre-treatment with TTO. Pre-treatment of astrocytes with 10 µM TTO markedly reduced JNK activation, when compared to astrocytes incubated with MPP alone (p < 0.05). Up-regulation of Bax and down-regulation of Bcl 2 by MPP in astrocytes were attenuated by pre-treatment with TTO. MPP-induced up-regulation of cleaved caspase 3 was suppressed in astrocytes by TTO pre-treatment (p < 0.05). Conclusion: Treatment with TTO prevents MPP+ -induced neuronal damage in vitro in astrocytes and in vivo in mice. The neuro-protective effect of TTO involves down-regulation of JNK activation, inhibition of caspase-3 level, decrease in Bax and increase in Bcl-2 expression. Thus, TTO has a potential for use in the treatment of Parkinson’s disease.

scholarly journals Adenosine Receptors as Neuroinflammation Modulators: Role of A1 Agonists and A2A Antagonists

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1739
Author(s):  
Aleix Martí Navia ◽  
Diego Dal Ben ◽  
Catia Lambertucci ◽  
Andrea Spinaci ◽  
Rosaria Volpini ◽  
...  
Keyword(s):  
Partial Agonist ◽  
Pathological Condition ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Potential Candidate ◽  
In Vivo Models ◽  
Tnf Α

The pathological condition of neuroinflammation is caused by the activation of the neuroimmune cells astrocytes and microglia. The autacoid adenosine seems to be an important neuromodulator in this condition. Its main receptors involved in the neuroinflammation modulation are A1AR and A2AAR. Evidence suggests that A1AR activation produces a neuroprotective effect and A2AARs block prevents neuroinflammation. The aim of this work is to elucidate the effects of these receptors in neuroinflammation using the partial agonist 2′-dCCPA (2-chloro-N6-cyclopentyl-2′-deoxyadenosine) (C1 KiA1AR = 550 nM, KiA2AAR = 24,800 nM, and KiA3AR = 5560 nM, α = 0.70, EC50A1AR = 832 nM) and the newly synthesized in house compound 8-chloro-9-ethyl-2-phenethoxyadenine (C2 KiA2AAR = 0.75 nM; KiA1AR = 17 nM and KiA3AR = 227 nM, IC50A2AAR = 251 nM unpublished results). The experiments were performed in in vitro and in in vivo models of neuroinflammation. Results showed that C1 was able to prevent the inflammatory effect induced by cytokine cocktail (TNF-α, IL-1β, and IFN-γ) while C2 possess both anti-inflammatory and antioxidant properties, counteracting both neuroinflammation in mixed glial cells and in an animal model of neuroinflammation. In conclusion, C2 is a potential candidate for neuroinflammation therapy.

The Neuroprotective Effect of Picroside II from Hu-Huang-Lian against Oxidative Stress

2007 ◽  
Vol 35 (04) ◽  
pp. 681-691 ◽  
Author(s):  
Ting Li ◽  
Jian-Wen Liu ◽  
Xiao-Dong Zhang ◽  
Ming-Chuan Guo ◽  
Guang Ji
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Therapeutic Potential ◽  
Neuroprotective Effect ◽  
Active Constituent ◽  
Sod Activity ◽  
Picroside Ii ◽  
Pre Treatment

Picroside II is an active constituent extracted from the traditional Chinese medicine (TCM) Hu-Huang-Lian. To evaluate the neuroprotective effect of picroside II, PC12 cells were treated with glutamate in vitro and male ICR mice were treated with AlCl 3in vivo. Pre-treatment of PC12 cells with picroside II could enhance the cell viability and decrease the level of intracellular reactive oxygen species (ROS) induced by glutamate. By DNA fragmentation and flow cytometry assay, picroside II (1.2 mg/ml) significantly prevented glutamate-induced cell apoptosis. In the animal study, amnesia was induced in mice by AlCl 3 (100 mg/kg/d, i.v.). Pricroside II, at the dose of 20 and 40 mg/kg/d (i.g.), markedly ameliorated AlCl 3-induced learning and memory dysfunctions and attenuated AlCl 3-induced histological changes. This was associated with the significant increased superoxide dismutase (SOD) activity in the brain of experimental mice. All these results indicated that picroside II possessed the therapeutic potential in protecting against neurological injuries damaged by oxidative stress.

scholarly journals Protective Effects of Aqueous Extract ofLuehea divaricataagainst Behavioral and Oxidative Changes Induced by 3-Nitropropionic Acid in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Aline Alves Courtes ◽  
Letícia Priscila Arantes ◽  
Rômulo Pillon Barcelos ◽  
Ingrid Kich da Silva ◽  
Aline Augusti Boligon ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Aqueous Extract ◽  
Antioxidant Properties ◽  
Male Rats ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Nitropropionic Acid ◽  
3 Nitropropionic Acid

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease. Accordingly, 3-nitropropionic acid (3-NP) has been found to effectively produce HD-like symptoms.Luehea divaricata(L. divaricata), popularly known in Brazil as “açoita-cavalo,” may act as a neuroprotective agentin vitroandin vivo. We evaluated the hypothesis that the aqueous extract ofL. divaricatacould prevent behavioral and oxidative alterations induced by 3-NP in rats. 25 adult Wistar male rats were divided into 5 groups: (1) control, (2)L. divaricata(1000 mg/kg), (3) 3-NP, (4)L. divaricata(500 mg/kg) + 3-NP, and (5)L. divaricata(1000 mg/kg) + 3-NP. Groups 2, 4, and 5 receivedL. divaricatavia intragastric gavage daily for 10 days. Animals in groups 3, 4, and 5 received 20 mg/kg 3-NP daily from days 8–10. At day 10, parameters of locomotor activity and biochemical evaluations were performed. Indeed, rats treated with 3-NP showed decreased locomotor activity compared to controls. Additionally, 3-NP increased levels of reactive oxygen species and lipid peroxidation and decreased ratio of GSH/GSSG and acetylcholinesterase activity in cortex and/or striatum. Our results suggest that rats pretreated withL. divaricataprior to 3-NP treatment showed neuroprotective effects when compared to 3-NP treated controls, which may be due to its antioxidant properties.

scholarly journals Antioxidant and Neuroprotective Properties of Eugenia dysenterica Leaves

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Douglas Vieira Thomaz ◽  
Luanna Fernandes Peixoto ◽  
Thiago Sardinha de Oliveira ◽  
James Oluwagbamigbe Fajemiroye ◽  
Hiasmin Franciely da Silva Neri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Electrode System ◽  
Antioxidant Compounds ◽  
Hydroalcoholic Extract ◽  
Markers Of Oxidative Stress ◽  
Eugenia Dysenterica

Eugenia dysenterica ex DC Mart. (Myrtaceae), popularly known as “cagaita,” is a Brazilian plant rich in polyphenols and other antioxidant compounds. Aiming to evaluate the potential use of cagaita in pathologies involving oxidative stress, such as neurodegenerative disorders, this study investigated its antioxidant potential and neuroprotective effect. Electrochemical approaches and aluminium-induced neurotoxicity were used to determine respectively in vitro and in vivo antioxidant properties of cagaita. Voltammetric experiments were carried out in a three-electrode system, whose working electrode consisted of glassy carbon. Male Swiss mice were administered with AlCl3 orally at a dose of 100 mg/kg/day and with cagaita leaf hydroalcoholic extract (CHE) at doses of 10, 100, and 300 mg/kg/day. The redox behavior of CHE presented similar features to that of quercetin, a widely known antioxidant standard. CHE prevented mouse memory impairment which resulted from aluminium intake. In addition, biochemical markers of oxidative stress (catalase, superoxide dismutase activity, and lipid peroxidation) were normalized by CHE treatment. The potential of CHE to prevent aluminium-induced neurotoxicity was reflected at the microscopic level, through the decrease of the number of eosinophilic necrosis phenotypes seen in treated groups. Moreover, the protective effect of CHE was similar to that of quercetin, which was taken as the standard. These findings showed that the CHE of cagaita leaves has a potential to protect the brain against oxidative-induced brain damage.

scholarly journals Role of Quercetin in Depressive-Like Behaviors: Findings from Animal Models

2021 ◽  
Vol 11 (15) ◽  
pp. 7116
Author(s):  
Serena Silvestro ◽  
Placido Bramanti ◽  
Emanuela Mazzon
Keyword(s):  
Animal Models ◽  
Fruits And Vegetables ◽  
Antioxidant Properties ◽  
Preclinical Studies ◽  
Neuroprotective Effects ◽  
Beneficial Effects ◽  
Novel Treatment ◽  
Pre Treatment ◽  
Vegetables And Fruits

Depressive-like behavior is a highly prevalent worldwide neuropsychiatric disorder that owns a complex pathophysiologic mechanism. The available pharmacotherapy is ineffective for most patients and shown several adverse effects. Therefore, it is important to find efficacy and safe antidepressive compounds. Some phytochemicals compounds regulate the same genes and pathways targeted by drugs; therefore, diets rich in fruits and vegetables could be considered novel treatment approaches. Currently, the functional properties of quercetin acquired great interest, due to its beneficial effects on health. Quercetin is a flavonoid ubiquitously present in vegetables and fruits, interestingly for its strong antioxidant properties. The purpose of this review is to summarize the preclinical studies present in the literature, in the last ten years, aimed at illustrating the effects of quercetin pre-treatment in depressive-like behaviors. Quercetin resulted in antidepressant-like actions due to its antioxidant, anti-inflammatory, and neuroprotective effects. This pointed out the usefulness of this flavonoid as a nutraceutical compound against the development of psychological stress-induced behavioral perturbation. Therefore, quercetin or a diet containing it may become a prospective supplementation or an efficient adjuvant therapy for preventing stress-mediated depressive-like behavior.

scholarly journals A New Look at the Bioactive Properties of Anthocyanin-rich Horticultural Crops

HortScience ◽  
1997 ◽  
Vol 32 (3) ◽  
pp. 555E-556
Author(s):  
M.A.L. Smith
Keyword(s):  
Animal Models ◽  
Fruits And Vegetables ◽  
Antioxidant Properties ◽  
In Vitro Assays ◽  
Total Serum ◽  
Total Serum Cholesterol ◽  
Horticultural Crops ◽  
Anthocyanin Pigments

The bright red pigmentation in edible, anthocyanin-rich fruits and vegetables is a definite bonus in terms of market appeal. As a result, breeders have worked consistently to intensify anthocyanin levels or alter composition in crops. The positive links between consumption of crops and food products containing natural anthocyanin pigments, and reduced incidence of cardiovascular and other chronic diseases, have been established anecdotally and more recently validated in research trials including those from our laboratory group. The protective events, most attributed to the potent antioxidant properties of anthocyanin pigments and associated phytochemicals, place anthocyanin-rich crops in the category of “Functional Foods,” yielding health protection unrelated to nutritional value. In vitro bioactivity assays have identified components from these crops capable of blocking the initiation stages of carcinogenesis, while a completely separate class of phytochemicals and sets of assays establish efficacy against the promotion stages of tumorigenesis. Animal models for carcinogen-induced damage to mammary gland and skin DNA subsequently demonstrate the in vivo potency of the same target compounds. Similarly, to establish cardioprotective properties, demonstrations of ability to inhibit platelet aggregation, relax vascular muscle tissue, and reduce total serum cholesterol are demonstrated in a series of in vitro assays, and via animal models and human studies. While activity-directed fractionations seek to identify specific responsible compounds, it is increasingly evident that bioactivity is drastically attenuated once specific compounds are isolated, and the synergistic interaction of associated phytochemicals in horticultural crops is prerequisite to realizing health benefits. These complications have slowed the establishment of effective minimum “dosages,” but all the more strongly promote consumption of the crops.

scholarly journals Montelukast Protects Against Renal Damage Due to Cadmium Toxicity: In vivo and In vitro Experiments

2021 ◽  
Vol 15 (4) ◽  
pp. 223-232
Author(s):  
Farnoosh Kaviani ◽  
◽  
Missagh Jalali ◽  
Elham Hoveizi ◽  
Javad Jamshidian ◽  
...  
Keyword(s):  
Vitamin E ◽  
Cell Damage ◽  
Cadmium Toxicity ◽  
Antioxidant Properties ◽  
Protective Effects ◽  
Human Embryonic Kidney Cells ◽  
Pre Treatment ◽  
Gpx Activity

Background: The protective effects of Montelukast (Mont), as an anti-inflammatory drug, against cadmium-induced kidney cell damage have already been studied and identified. Since the significant part of cadmium nephrotoxicity is caused by oxidative stress, this in vivo and in vitro study was conducted to investigate the possible role of Montelukast antioxidant properties in the protection. Methods: In the in vivo section, 42 rats were treated in seven groups of six rats as follows: Control; Cadmium Chloride (CdCl2) control; Montelukast control; CdCl2 plus Montelukast treatment; CdCl2 with Montelukast pre-treatment; Vitamin E control; CdCl2 plus Vitamin E treatment. In the in vitro section, human embryonic kidney cells (HEK293) were treated with CdCl2; Montelukast; Combined CdCl2 and Montelukast; Vitamin E; Combined CdCl2 and Vitamin E. Results: Montelukast, in both treatment and pretreatment forms, reduced serum urea, creatinine, and potassium levels compared to CdCl2 group, in vivo. Similar to vitamin E, the pre-treatment with Montelukast was associated with a significant decrease in Nitric Oxide (NO) and Total Antioxidant Capacity (TAC) in serum and renal tissue, and a significant increase in Glutathione Peroxidase (GPX) activity in serum compared those in the CdCl2 group. In the in vitro section of the study, Montelukast significantly reduced Malondialdehyde (MDA) and NO while the TAC level, Superoxide Dismutase (SOD), and the GPX activity increased significantly. Conclusion: Overall, the antioxidant effects of Montelukast appear to play a prominent role in preventing the renal toxicity due to cadmium exposure.

Resveratrol Reduces Matrix Metalloproteinase-2 Activity Induced by Oxygen-Glucose Deprivation and Reoxygenation in Human Cerebral Microvascular Endothelial Cells

2012 ◽  
Vol 82 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Zahide Cavdar ◽  
Mehtap Y. Egrilmez ◽  
Zekiye S. Altun ◽  
Nur Arslan ◽  
Nilgun Yener ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Neurovascular Unit ◽  
Glucose Deprivation ◽  
Matrix Metalloproteinase 2 ◽  
Microvascular Endothelial Cells ◽  
Oxygen Glucose Deprivation ◽  
Microvascular Endothelial

The main pathophysiology in cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Among the human matrix metalloproteinases (MMPs), MMP-2 and -9, known as gelatinases, are the key enzymes for degrading type IV collagen, which is the major component of the basal membrane that surrounds the cerebral blood vessel. In the present study, we investigated the effects of resveratrol on cytotoxicity, reactive oxygen species (ROS), and gelatinases (MMP-2 and -9) in human cerebral microvascular endothelial cells exposed to 6 hours of oxygen-glucose deprivation and a subsequent 24 hours of reoxygenation with glucose (OGD/R), to mimic ischemia/reperfusion in vivo. Lactate dehydrogenase increased significantly, in comparison to that in the normoxia group. ROS was markedly increased in the OGD/R group, compared to normoxia. Correspondingly, ROS was significantly reduced with 50 μM of resveratrol. The proMMP-2 activity in the OGD/R group showed a statistically significant increase from the control cells. Resveratrol preconditioning decreased significantly the proMMP-2 in the cells exposed to OGD/R in comparison to that in the OGD/R group. Our results indicate that resveratrol regulates MMP-2 activity induced by OGD/R via its antioxidant effect, implying a possible mechanism related to the neuroprotective effect of resveratrol.

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