Epalrestat improves motor symptoms by reducing oxidative stress and inflammation in the reserpine induced mouse model of Parkinson's disease.

Epalrestat Parkinson's disease bradykinesia glutathione oxidative‐stress

Journal

Animal models and experimental medicine
ISSN: 2576-2095
Titre abrégé: Animal Model Exp Med
Pays: United States
ID NLM: 101726292

Informations de publication

Date de publication:
Mar 2020
Historique:
received: 07 09 2019
revised: 12 11 2019
accepted: 06 12 2019
entrez: 23 4 2020
pubmed: 23 4 2020
medline: 23 4 2020
Statut: epublish

Résumé

Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting a large number of elderly people worldwide. The current therapies for PD are symptom-based; they do not provide a cure but improve the quality of life. Muscular dysfunction is the hallmark clinical feature of PD and oxidative stress and inflammation play a critical role in its pathogenesis. Epalrestat is used for the treatment of diabetic neuropathy and is known to improve antioxidative defense mechanisms in the CNS. Therefore, in this study, we investigated the role of Epalrestat in the reserpine induced mouse model of PD. We used Swiss Albino mice for the PD model and tested for akinesia/bradykinesia, muscular rigidity, palpebral ptosis, and tremor, as well as conducting swim and open field tests. Brain samples were used to determine oxidative stress parameters and infiltration of immune cells. Epalrestat treatment significantly improved akinesia and bradykinesia, muscular dysfunctions, tremor level, and gait functions compared to the reserpine group. It also improved the latency in the swim test. Eplarestat significantly reduced lipid peroxidation and NO concentration in different brain tissues and increased the activity of antioxidative enzymes, glutathione, catalase, and superoxide dismutase. Furthermore, Epalrestat reduced neuroinflammation by reducing the number of infiltrating immune cells. Eplarestat improves muscular dysfunction in PD by reducing oxidative stress and inflammation.

Sections du résumé

BACKGROUND BACKGROUND
Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting a large number of elderly people worldwide. The current therapies for PD are symptom-based; they do not provide a cure but improve the quality of life. Muscular dysfunction is the hallmark clinical feature of PD and oxidative stress and inflammation play a critical role in its pathogenesis. Epalrestat is used for the treatment of diabetic neuropathy and is known to improve antioxidative defense mechanisms in the CNS. Therefore, in this study, we investigated the role of Epalrestat in the reserpine induced mouse model of PD.
METHOD METHODS
We used Swiss Albino mice for the PD model and tested for akinesia/bradykinesia, muscular rigidity, palpebral ptosis, and tremor, as well as conducting swim and open field tests. Brain samples were used to determine oxidative stress parameters and infiltration of immune cells.
RESULTS RESULTS
Epalrestat treatment significantly improved akinesia and bradykinesia, muscular dysfunctions, tremor level, and gait functions compared to the reserpine group. It also improved the latency in the swim test. Eplarestat significantly reduced lipid peroxidation and NO concentration in different brain tissues and increased the activity of antioxidative enzymes, glutathione, catalase, and superoxide dismutase. Furthermore, Epalrestat reduced neuroinflammation by reducing the number of infiltrating immune cells.
CONCLUSION CONCLUSIONS
Eplarestat improves muscular dysfunction in PD by reducing oxidative stress and inflammation.

Identifiants

pubmed: 32318655
doi: 10.1002/ame2.12097
pii: AME212097
pmc: PMC7167235
doi:

Types de publication

Journal Article

Langues

eng

Pagination

9-21

Informations de copyright

© 2019 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences.

Déclaration de conflit d'intérêts

None.

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Auteurs

Md Mahbubur Rahman (MM)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Rupali Rani Chakraborti (RR)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Md Abdullah Potol (MA)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Ariful Haque Abir (AH)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Ozayra Sharmin (O)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Mahabub Alam (M)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Md Fazlur Rahman Khan (MFR)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Rownock Afrin (R)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Humayra Jannat (H)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Rasiqh Wadud (R)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Zaki Farhad Habib (ZF)

Laboratory of Pharmacology Department of Pharmaceutical Sciences School of Health & Life Sciences North South University Dhaka Bangladesh.

Classifications MeSH