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How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway

Aluminum phosphide (ALP) is among the most significant causes of brain toxicity and death in many countries. Curcumin (CUR), a major turmeric component, is a potent protective agent against many diseases, including brain toxicity. This study aimed to examine the probable protection potential of nano...

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Autores principales: Khodavysi, Milad, Kheiripour, Nejat, Ghasemi, Hassan, Soleimani-Asl, Sara, Jouzdani, Ali Fathi, Sabahi, Mohammadmahdi, Ganji, Zahra, Azizi, Zahra, Ranjbar, Akram
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AIMS Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106336/
https://www.ncbi.nlm.nih.gov/pubmed/37077959
http://dx.doi.org/10.3934/Neuroscience.2023005
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author Khodavysi, Milad
Kheiripour, Nejat
Ghasemi, Hassan
Soleimani-Asl, Sara
Jouzdani, Ali Fathi
Sabahi, Mohammadmahdi
Ganji, Zahra
Azizi, Zahra
Ranjbar, Akram
author_facet Khodavysi, Milad
Kheiripour, Nejat
Ghasemi, Hassan
Soleimani-Asl, Sara
Jouzdani, Ali Fathi
Sabahi, Mohammadmahdi
Ganji, Zahra
Azizi, Zahra
Ranjbar, Akram
author_sort Khodavysi, Milad
collection PubMed
description Aluminum phosphide (ALP) is among the most significant causes of brain toxicity and death in many countries. Curcumin (CUR), a major turmeric component, is a potent protective agent against many diseases, including brain toxicity. This study aimed to examine the probable protection potential of nanomicelle curcumin (nanomicelle-CUR) and its underlying mechanism in a rat model of ALP-induced brain toxicity. A total of 36 Wistar rats were randomly divided into six groups (n = 6) and exposed to ALP (2 mg/kg/day, orally) + CUR or nanomicelle-CUR (100 mg/kg/day, orally) for 7 days. Then, they were anesthetized, and brain tissue samples were dissected to evaluate histopathological alterations, oxidative stress biomarkers, gene expression of SIRT1, FOXO1a, FOXO3a, CAT and GPX in brain tissue via hematoxylin and eosin (H&E) staining, biochemical and enzyme-linked immunosorbent assay (ELISA) methods and Real-Time PCR analysis. CUR and nanomicelle-CUR caused significant improvement in ALP-induced brain damage by reducing the MDA levels and induction of antioxidant capacity (TTG, TAC and SOD levels) and antioxidant enzymes (CAT, GPX), modulation of histopathological changes and up-regulation of gene expression of SIRT1 in brain tissue. It was concluded that nanomicelle-CUR treatment ameliorated the harmful effects of ALP-induced brain toxicity by reducing oxidative stress. Therefore, it could be considered a suitable therapeutic choice for ALP poisoning.
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spelling pubmed-101063362023-04-18 How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway Khodavysi, Milad Kheiripour, Nejat Ghasemi, Hassan Soleimani-Asl, Sara Jouzdani, Ali Fathi Sabahi, Mohammadmahdi Ganji, Zahra Azizi, Zahra Ranjbar, Akram AIMS Neurosci Research Article Aluminum phosphide (ALP) is among the most significant causes of brain toxicity and death in many countries. Curcumin (CUR), a major turmeric component, is a potent protective agent against many diseases, including brain toxicity. This study aimed to examine the probable protection potential of nanomicelle curcumin (nanomicelle-CUR) and its underlying mechanism in a rat model of ALP-induced brain toxicity. A total of 36 Wistar rats were randomly divided into six groups (n = 6) and exposed to ALP (2 mg/kg/day, orally) + CUR or nanomicelle-CUR (100 mg/kg/day, orally) for 7 days. Then, they were anesthetized, and brain tissue samples were dissected to evaluate histopathological alterations, oxidative stress biomarkers, gene expression of SIRT1, FOXO1a, FOXO3a, CAT and GPX in brain tissue via hematoxylin and eosin (H&E) staining, biochemical and enzyme-linked immunosorbent assay (ELISA) methods and Real-Time PCR analysis. CUR and nanomicelle-CUR caused significant improvement in ALP-induced brain damage by reducing the MDA levels and induction of antioxidant capacity (TTG, TAC and SOD levels) and antioxidant enzymes (CAT, GPX), modulation of histopathological changes and up-regulation of gene expression of SIRT1 in brain tissue. It was concluded that nanomicelle-CUR treatment ameliorated the harmful effects of ALP-induced brain toxicity by reducing oxidative stress. Therefore, it could be considered a suitable therapeutic choice for ALP poisoning. AIMS Press 2023-04-04 /pmc/articles/PMC10106336/ /pubmed/37077959 http://dx.doi.org/10.3934/Neuroscience.2023005 Text en © 2023 the Author(s), licensee AIMS Press https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/) )
spellingShingle Research Article
Khodavysi, Milad
Kheiripour, Nejat
Ghasemi, Hassan
Soleimani-Asl, Sara
Jouzdani, Ali Fathi
Sabahi, Mohammadmahdi
Ganji, Zahra
Azizi, Zahra
Ranjbar, Akram
How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title_full How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title_fullStr How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title_full_unstemmed How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title_short How can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: Role of SIRT1/FOXO3 signaling pathway
title_sort how can nanomicelle-curcumin modulate aluminum phosphide-induced neurotoxicity?: role of sirt1/foxo3 signaling pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10106336/
https://www.ncbi.nlm.nih.gov/pubmed/37077959
http://dx.doi.org/10.3934/Neuroscience.2023005
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