Dose Dependent Effects of Breynia cernua Against the Paraquat Induced Parkinsonism like Symptoms in Animals’ Model: In Vitro , In Vivo and Mechanistic Studies

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Abstract

The aims and objectives of the study were to evaluate the antiParkinson’s (PD) potential of B cernua (BCE). B cernua (Poir.) Müll. Arg. (B cernua) is a member of the Phyllanthaceae family. HPLC revealed the presence of various phytochemicals. Study was conducted for 40 days. After PD induction by paraquat behavioural studies were carried out. Biochemical parameters such as DPPH, NO-scavenging, Ferrous reducing power, MDA, GSH, CAT, SOD, acetylcholinesterase (AChE), neurotransmitter estimation and TNF-α and IL-6 levels were determined. DPPH, NO-scavenging and Ferrous reducing power assays showed 78.02%, 48.05% and 71.45% inhibitions, respectively. There was significant improvement in motor functions and coordination in a dose-dependent manner (50 < 250 < 500 mg/kg) in PD rat model. Biochemical markers; SOD, CAT, GPx and GSH showed significant restoration ( P < .001) while MDA showed significant decrease ( P < .05). The AChE level was significantly reduced ( P < .05) at 500 mg/kg while neurotransmitters were significantly improved ( P < .001) in a dose-dependent fashion. The ELISA results showed significant ( P < .001) down-regulation of IL-6 and TNF-α level. In conclusion, it is suggested that BCE has the potential to reduce the symptoms of PD.

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Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis.

Claire Henchcliffe, M. Beal (2008)

Parkinson disease (PD) is associated with progressive loss of dopaminergic neurons in the substantia nigra, as well as with more-widespread neuronal changes that cause complex and variable motor and nonmotor symptoms. Recent rapid advances in PD genetics have revealed a prominent role for mitochondrial dysfunction in the pathogenesis of the disease, and the products of several PD-associated genes, including SNCA, Parkin, PINK1, DJ-1, LRRK2 and HTR2A, show a degree of localization to the mitochondria under certain conditions. Impaired mitochondrial function is likely to increase oxidative stress and might render cells more vulnerable to this and other related processes, including excitotoxicity. The mitochondria, therefore, represent a highly promising target for the development of disease biomarkers by use of genetic, biochemical and bioimaging approaches. Novel therapeutic interventions that modify mitochondrial function are currently under development, and a large phase III clinical trial is underway to examine whether high-dose oral coenzyme Q10 will slow disease progression. In this Review, we examine evidence for the roles of mitochondrial dysfunction and increased oxidative stress in the neuronal loss that leads to PD and discuss how this knowledge might further improve patient management and aid in the development of 'mitochondrial therapy' for PD.

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Non-motor symptoms of Parkinson's disease: dopaminergic pathophysiology and treatment.

K Chaudhuri, Anthony HV Schapira (2009)

Several studies, including work from the Parkinson's disease (PD) non-motor group and others, have established that the non-motor symptoms of PD are common, occur across all stages of PD, are under-reported, and are a key determinant of quality of life. Research suggests that the non-motor symptoms of the disease are frequently unrecognised by clinicians and remain untreated. Even when identified, there is a common perception that many of these symptoms are untreatable. The role of dopaminergic drugs in treating the various non-motor problems of PD, although clinically recognised, has received little attention. In this Review, we investigate the dopaminergic basis of the range of non-motor symptoms that occur in PD such as depression, apathy, sleep disorders (including rapid-eye movement sleep behaviour disorder), and erectile dysfunction. We discuss the evidence that these symptoms are treatable, at least in part, with various dopaminergic strategies and, where relevant, we also refer to the use of deep-brain stimulation of appropriate targets in the brain. This Review provides a comprehensive overview of the management of this challenging aspect of PD.

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Cellular Senescence Is Induced by the Environmental Neurotoxin Paraquat and Contributes to Neuropathology Linked to Parkinson’s Disease

Shankar J. Chinta, Georgia Woods, Marco Demaria … (2018)

SUMMARY Exposure to the herbicide paraquat (PQ) is associated with an increased risk of idiopathic Parkinson’s disease (PD). Therapies based on PQ’s presumed mechanisms of action have not, however, yielded effective disease therapies. Cellular senescence is an anticancer mechanism that arrests proliferation of replication-competent cells and results in a pro-inflammatory senescence-associated secretory phenotype (SASP) capable of damaging neighboring tissues. Here, we demonstrate that senescent cell markers are preferentially present within astrocytes in PD brain tissues. Additionally, PQ was found to induce astrocytic senescence and an SASP in vitro and in vivo, and senescent cell depletion in the latter protects against PQ-induced neuropathology. Our data suggest that exposure to certain environmental toxins promotes accumulation of senescent cells in the aging brain, which can contribute to dopaminergic neurodegeneration. Therapies that target senescent cells may constitute a strategy for treatment of sporadic PD, for which environmental exposure is a major risk factor.

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Journal ID (nlm-ta): Dose Response

Journal ID (iso-abbrev): Dose Response

Journal ID (hwp): spdos

Journal ID (publisher-id): DOS

Title: Dose-Response

Publisher: SAGE Publications (Sage CA: Los Angeles, CA )

ISSN (Electronic): 1559-3258

Publication date (Electronic): 9 September 2022

Publication date Collection: Jul-Sep 2022

Volume: 20

Issue: 3

Electronic Location Identifier: 15593258221125478

Affiliations

[1 ]Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, universityGovernment College University, , Ringgold 72594; Faisalabad, Pakistan

[2 ]Department of Pharmacology, Faculty of Pharmaceutical Sciences, universityGovernment College University, , Ringgold 72594; Faisalabad, Pakistan

[3 ]Department of Pharmacology, Faculty of Pharmacy, Ringgold 54735, universityThe Islamia University of Bahawalpur; , Pakistan

[4 ]Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Ringgold 54735, universityThe Islamia University of Bahawalpur; , Pakistan

Author notes

[*]Liaqat Hussain, Department of Pharmacology, Faculty of Pharmaceutical Sciences, Government College University, Allama Iqbal Road, Faisalabad 38000, Pakistan. Email: liaqat.hussain@ 123456gcuf.edu.pk

[*]Malik Saadullah, Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences, Government College University, Allama Iqbal Road, Faisalabad 38000, Pakistan. Email: maliksaaadullah@ 123456gcuf.edu.pk

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Liaqat Hussain https://orcid.org/0000-0001-7171-5917

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Publisher ID: 10.1177_15593258221125478

DOI: 10.1177/15593258221125478

PMC ID: 9465616

PubMed ID: 36106058

SO-VID: 43ffe7b4-261e-4b92-9150-d8caae464db5

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This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

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typesetter ts10

cover-date July-September 2022

Keywords: breynia cernua,phyllanthaceae,parkinson’s disease,paraquat,glycosides,saponins

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Keywords: breynia cernua, phyllanthaceae, parkinson’s disease, paraquat, glycosides, saponins

Dose Dependent Effects of Breynia cernua Against the Paraquat Induced Parkinsonism like Symptoms in Animals’ Model: In Vitro , In Vivo and Mechanistic Studies

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Herbal Medicines Journal (Herb Med J)

Most cited references 56

Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis.

Non-motor symptoms of Parkinson's disease: dopaminergic pathophysiology and treatment.

Cellular Senescence Is Induced by the Environmental Neurotoxin Paraquat and Contributes to Neuropathology Linked to Parkinson’s Disease

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