Effects of Quercetin on Neurodegenerative and Compensatory Processes in the Nigrostriatal System in a Model of the Preclinical Stage of Parkinson’s Disease in Rats

Екимова, И. В.; Plaksina, D. V.

doi:10.1007/s11055-017-0508-x

Cited by 9 publications

(9 citation statements)

References 21 publications

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“…Previous evidence has shown that LAC could lead to retrograde accumulation of α-syn in vivo (Laser et al, 2003;Miwa et al, 2005) and ubiquitin-and α-syn-positive inclusions in both TH+ and non-TH+ neurons in vitro and in vivo, suggesting that the accumulation of α-syn can occur in non-dopaminergic neurons after injection of LAC or other proteasome inhibitors (Rideout et al, 2005;Ebrahimi-Fakhari et al, 2011;Bentea et al, 2015). In the same way, intranasal administration of high levels of LAC led to a decrease in the number of dopaminergic neurons in the OB and SNc of rats (Ekimova et al, 2016;Ekimova and Plaksina, 2017). Thus, we hypothesized whether long-term proteasome inhibition in regions of the brain of (E-G) OB and stained with α-syn are shown.…”

Section: Discussionmentioning

confidence: 90%

Lack of Parkinsonian Pathology and Neurodegeneration in Mice After Long-Term Injections of a Proteasome Inhibitor in Olfactory Bulb and Amygdala

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Balzano

Martin-Rodriguez

et al. 2021

Front. Aging Neurosci.

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Proteinaceous inclusions, called Lewy bodies (LBs), are used as a pathological hallmark for Parkinson’s disease (PD). Recent studies suggested a prion-like spreading mechanism for α-synucleinopathy where early neuropathological deposits occur, among others, in the olfactory bulb (OB) and amygdala. LBs contain insoluble α-synuclein and many other ubiquitinated proteins, suggesting a role of protein degradation system failure in PD pathogenesis. Therefore, we wanted to study the effects of a proteasomal inhibitor, lactacystin, on the aggregability and transmissibility of α-synuclein in the OB and amygdala. We performed injections of lactacystin in the OB and amygdala of wild-type mice. Motor behavior, markers of neuroinflammation, α-synuclein, and dopaminergic integrity were assessed by immunohistochemistry. Overall, there were no differences in the number of neurons and α-synuclein expression in these regions following injection of lactacystin into either the OB or amygdala. Microglial and astroglial labeling appeared to be correlated with surgery-induced inflammation or local effects of lactacystin. Consistent with the behavior and pathological findings, there was no loss of dopaminergic cell bodies in the substantia nigra and terminals in the striatum. Our data showed that long-term lactacystin injections in extra nigrostriatal regions may not mimic spreading aspects of PD and reinforce the special vulnerability of dopaminergic neurons of the substantia nigra pars compacta (SNc).

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Section: Discussionmentioning

confidence: 90%

Lack of Parkinsonian Pathology and Neurodegeneration in Mice After Long-Term Injections of a Proteasome Inhibitor in Olfactory Bulb and Amygdala

provided

Balzano

Martin-Rodriguez

et al. 2021

Front. Aging Neurosci.

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“…Research of Ekimova at al. (30) carried out on experimental animals prove that anti-diabetic, antioxidant and acetylcholine esterase (AChE) inhibitors have beneficial effects on diabetic neurodegenerative disease, particularly on memory damage and cognitive dysfunction (30). Studies on various in vivo models (9.30, 31) confirm the neuro-protective effects of QE.…”

Section: Quercetin and Diabetic Neurodegenerative Diseasesmentioning

confidence: 99%

The effect of quercetin on diabetis complications

2020

HORIZONS

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Diabetes is a serious metabolic disorder with a numerous complications and one of the five leading causes of death worldwide. Diabetes, so called "soft killer" is characterized by persistent hyperglycemia associated with carbohydrate, protein, and lipid metabolism abnormalities. However, the currently available diabetic drugs have numerous limitations because of their side effects including hypoglycemia, cell death, and high rates of secondary alterations. Recently, emphasis has been placed on complementary and alternative treatments for diabetes focused on functional food and its bioactive compounds. One of them is quercetin, a powerful antioxidant flavonoid, which posseses various biochemical and physiological effects (anti-diabetic, antioxidant and anti-inflammatory). The aim of this study is a literature review focused on the impact of quercetin on diabetic complications. In vivo and in vitro studies suggest that quercetin is a promising bioactive compound for treatment of this disease, but its efficacy should be confirmed by clinical trials.

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“…Considering all administration routes, QUE concentration dosage ranged from 6 μM to 400 mg/kg (Tables 2 and 3). IP administration doses ranged from 5 mg/kg 12,15,31,37 to 200 mg/kg. 8,30,41,48 The highest free QUE dose found (400 mg/kg) was administered PO, and it did not result in significant improvements in neuronal function, histological parameters and behavioural outcomes when compared to the PD group.…”

Section: Que Treatmentsmentioning

confidence: 99%

“…57 LC-induced PD and MitoPark transgenic mice were the most uncommon choices found in our search. 31,59 LC is a proteasome inhibitor that leads to the loss of nigrostriatal dopaminergic neurons due to their high content of heat shock protein 70 (HSP70), also inducing the formation of α-synuclein aggregates. 60 Interestingly, QUE treatment in a LC-induced PD model led to a 1.5-fold increase in the loss of dopaminergic neurons in comparison to LC alone.…”

Section: Animal Models For Pdmentioning

confidence: 99%

“…60 Interestingly, QUE treatment in a LC-induced PD model led to a 1.5-fold increase in the loss of dopaminergic neurons in comparison to LC alone. 31 The MitoPark mouse, on the other hand, is a transgenic model that start showing compromised locomotor activity from 12 weeks of age, accompanied by the progressive loss of dopaminergic neurons in the SNC that results in a reduction of dopamine in the striatum, reflecting nigrostriatal Average score: 7.08…”

Section: Animal Models For Pdmentioning

confidence: 99%

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Effects of quercetin in preclinical models of Parkinson's disease: A systematic review

de Oliveira Vian,

Marinho,

da Silva Marques

et al. 2024

Basic Clin Pharma Tox

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Parkinson's disease (PD) is a neurodegenerative disease that affects dopaminergic neurons, thus impairing dopaminergic signalling. Quercetin (QUE) has antioxidant and neuroprotective properties that are promising for the treatment of PD. This systematic review aimed to investigate the therapeutic effects of QUE against PD in preclinical models. The systematic search was performed in PubMed, Scopus and Web of Science. At the final screening stage, 26 articles were selected according to pre‐established criteria. Selected studies used different methods for PD induction, as well as animal models. Most studies used rats (73.08%) and mice (23.08%), with 6‐OHDA as the main strategy for PD induction (38.6%), followed by rotenone (30.8%). QUE was tested immersed in oil, nanosystems or in free formulations, in varied routes of administration and doses, ranging from 10 to 400 mg/kg and from 5 to 200 mg/kg in oral and intraperitoneal administrations, respectively. Overall, evidence from published data suggests a potential use of QUE as a treatment for PD, mainly through the inhibition of oxidative stress, neuroinflammatory response and apoptotic pathways.

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Effects of Quercetin on Neurodegenerative and Compensatory Processes in the Nigrostriatal System in a Model of the Preclinical Stage of Parkinson’s Disease in Rats

Cited by 9 publications

References 21 publications

Lack of Parkinsonian Pathology and Neurodegeneration in Mice After Long-Term Injections of a Proteasome Inhibitor in Olfactory Bulb and Amygdala

Lack of Parkinsonian Pathology and Neurodegeneration in Mice After Long-Term Injections of a Proteasome Inhibitor in Olfactory Bulb and Amygdala

The effect of quercetin on diabetis complications

Effects of quercetin in preclinical models of Parkinson's disease: A systematic review

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