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Inhibition of Oxidative Stress and the NF-κB Pathway by a Vitamin E Derivative: Pharmacological Approach against Parkinson’s Disease
[Image: see text] Parkinson’s disease (PD) is a progressive neurodegenerative disorder. In this study, PD was induced via (ip) injection of haloperidol (1 mg/kg/day). Animals were divided into seven groups (n = 70). Group I received the vehicle carboxymethylcellulose (CMC; 0.5%), group II was treate...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753179/ https://www.ncbi.nlm.nih.gov/pubmed/36530334 http://dx.doi.org/10.1021/acsomega.2c05500 |
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author | Iqbal, Afshan Anwar, Fareeha Saleem, Uzma Khan, Saira Sami Karim, Adnan Ahmad, Bashir Gul, Mubashra Iqbal, Zafer Ismail, Tariq |
author_facet | Iqbal, Afshan Anwar, Fareeha Saleem, Uzma Khan, Saira Sami Karim, Adnan Ahmad, Bashir Gul, Mubashra Iqbal, Zafer Ismail, Tariq |
author_sort | Iqbal, Afshan |
collection | PubMed |
description | [Image: see text] Parkinson’s disease (PD) is a progressive neurodegenerative disorder. In this study, PD was induced via (ip) injection of haloperidol (1 mg/kg/day). Animals were divided into seven groups (n = 70). Group I received the vehicle carboxymethylcellulose (CMC; 0.5%), group II was treated with designated 1 mg/kg haloperidol, and group III received the standard drug Sinemet (100 mg/kg), while groups IV–VII received a tocopherol derivative (Toco-D) at dose levels of 5, 10, 20, and 40 mg/kg, respectively, via the oral route. All groups received haloperidol for 23 consecutive days after their treatments except the control group. The improvement in locomotor activity and motor coordination was evaluated by using behavioral tests. Oxidative stress markers, neurotransmitters, and monoamine oxidase B (MAO-B) as well as NF-κB levels in the whole brain were measured. mRNA expression analysis of α-synuclein was carried out using the PCR technique. Toco-D at 20 mg/kg showed the maximum improvement in locomotor activity. The levels of antioxidant enzymes and neurotransmitters were also increased by the treatment with Toco-D. Inflammatory cytokine levels and mRNA expression of α-synuclein were decreased by Toco-D in treated animals. This study concluded that Toco-D might be effective in the improvement of locomotor activity and motor coordination in haloperidol-induced PD. |
format | Online Article Text |
id | pubmed-9753179 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-97531792022-12-16 Inhibition of Oxidative Stress and the NF-κB Pathway by a Vitamin E Derivative: Pharmacological Approach against Parkinson’s Disease Iqbal, Afshan Anwar, Fareeha Saleem, Uzma Khan, Saira Sami Karim, Adnan Ahmad, Bashir Gul, Mubashra Iqbal, Zafer Ismail, Tariq ACS Omega [Image: see text] Parkinson’s disease (PD) is a progressive neurodegenerative disorder. In this study, PD was induced via (ip) injection of haloperidol (1 mg/kg/day). Animals were divided into seven groups (n = 70). Group I received the vehicle carboxymethylcellulose (CMC; 0.5%), group II was treated with designated 1 mg/kg haloperidol, and group III received the standard drug Sinemet (100 mg/kg), while groups IV–VII received a tocopherol derivative (Toco-D) at dose levels of 5, 10, 20, and 40 mg/kg, respectively, via the oral route. All groups received haloperidol for 23 consecutive days after their treatments except the control group. The improvement in locomotor activity and motor coordination was evaluated by using behavioral tests. Oxidative stress markers, neurotransmitters, and monoamine oxidase B (MAO-B) as well as NF-κB levels in the whole brain were measured. mRNA expression analysis of α-synuclein was carried out using the PCR technique. Toco-D at 20 mg/kg showed the maximum improvement in locomotor activity. The levels of antioxidant enzymes and neurotransmitters were also increased by the treatment with Toco-D. Inflammatory cytokine levels and mRNA expression of α-synuclein were decreased by Toco-D in treated animals. This study concluded that Toco-D might be effective in the improvement of locomotor activity and motor coordination in haloperidol-induced PD. American Chemical Society 2022-12-02 /pmc/articles/PMC9753179/ /pubmed/36530334 http://dx.doi.org/10.1021/acsomega.2c05500 Text en © 2022 The Authors. Published by American Chemical Society https://creativecommons.org/licenses/by-nc-nd/4.0/Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works (https://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Iqbal, Afshan Anwar, Fareeha Saleem, Uzma Khan, Saira Sami Karim, Adnan Ahmad, Bashir Gul, Mubashra Iqbal, Zafer Ismail, Tariq Inhibition of Oxidative Stress and the NF-κB Pathway by a Vitamin E Derivative: Pharmacological Approach against Parkinson’s Disease |
title | Inhibition of Oxidative
Stress and the NF-κB
Pathway by a Vitamin E Derivative: Pharmacological Approach against
Parkinson’s Disease |
title_full | Inhibition of Oxidative
Stress and the NF-κB
Pathway by a Vitamin E Derivative: Pharmacological Approach against
Parkinson’s Disease |
title_fullStr | Inhibition of Oxidative
Stress and the NF-κB
Pathway by a Vitamin E Derivative: Pharmacological Approach against
Parkinson’s Disease |
title_full_unstemmed | Inhibition of Oxidative
Stress and the NF-κB
Pathway by a Vitamin E Derivative: Pharmacological Approach against
Parkinson’s Disease |
title_short | Inhibition of Oxidative
Stress and the NF-κB
Pathway by a Vitamin E Derivative: Pharmacological Approach against
Parkinson’s Disease |
title_sort | inhibition of oxidative
stress and the nf-κb
pathway by a vitamin e derivative: pharmacological approach against
parkinson’s disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753179/ https://www.ncbi.nlm.nih.gov/pubmed/36530334 http://dx.doi.org/10.1021/acsomega.2c05500 |
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