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Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study

Aluminum, one of the most abundant metallic elements, is known to be toxic to multiple organs including the kidneys. This study aimed to investigate the pleiotropic nephroprotective effects of Hesperidin in aluminum chloride (ALCL3)-induced renal injury, highlighting the potential molecular mechanis...

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Autores principales: Hassan, Nancy Husseiny, Yousef, Doaa Mohammed, Alsemeh, Amira Ebrahim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10039835/
https://www.ncbi.nlm.nih.gov/pubmed/36547838
http://dx.doi.org/10.1007/s11356-022-24800-0
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author Hassan, Nancy Husseiny
Yousef, Doaa Mohammed
Alsemeh, Amira Ebrahim
author_facet Hassan, Nancy Husseiny
Yousef, Doaa Mohammed
Alsemeh, Amira Ebrahim
author_sort Hassan, Nancy Husseiny
collection PubMed
description Aluminum, one of the most abundant metallic elements, is known to be toxic to multiple organs including the kidneys. This study aimed to investigate the pleiotropic nephroprotective effects of Hesperidin in aluminum chloride (ALCL3)-induced renal injury, highlighting the potential molecular mechanisms underlying. Twenty-four male albino rats were divided into four groups: control, Hesperidin (80 mg/kg BW, orally), ALCL3 (10 mg/kg BW, IP), and ALCL3 + Hesperidin groups. By the end of the study, blood samples were collected, and tissue samples were harvested at sacrifice. ALCL3 rats showed dramatically declined renal function, enhanced intrarenal oxidative stress, inflammation, apoptosis, and extravagant renal histopathological damage with interstitial fibrosis as shown by a higher Endothelial, Glomerular, Tubular, and Interstitial (EGTI) score. Hesperidin significantly reversed all the aforementioned detrimental effects in ALCL3-treated rats. The study verified the nephroprotective effects of Hesperidin on ALCL3-induced renal damage and confirmed the critical role of extracellular matrix (ECM) remodeling and apoptosis inhibition. GRAPHICAL ABSTRACT: [Image: see text]
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spelling pubmed-100398352023-03-27 Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study Hassan, Nancy Husseiny Yousef, Doaa Mohammed Alsemeh, Amira Ebrahim Environ Sci Pollut Res Int Research Article Aluminum, one of the most abundant metallic elements, is known to be toxic to multiple organs including the kidneys. This study aimed to investigate the pleiotropic nephroprotective effects of Hesperidin in aluminum chloride (ALCL3)-induced renal injury, highlighting the potential molecular mechanisms underlying. Twenty-four male albino rats were divided into four groups: control, Hesperidin (80 mg/kg BW, orally), ALCL3 (10 mg/kg BW, IP), and ALCL3 + Hesperidin groups. By the end of the study, blood samples were collected, and tissue samples were harvested at sacrifice. ALCL3 rats showed dramatically declined renal function, enhanced intrarenal oxidative stress, inflammation, apoptosis, and extravagant renal histopathological damage with interstitial fibrosis as shown by a higher Endothelial, Glomerular, Tubular, and Interstitial (EGTI) score. Hesperidin significantly reversed all the aforementioned detrimental effects in ALCL3-treated rats. The study verified the nephroprotective effects of Hesperidin on ALCL3-induced renal damage and confirmed the critical role of extracellular matrix (ECM) remodeling and apoptosis inhibition. GRAPHICAL ABSTRACT: [Image: see text] Springer Berlin Heidelberg 2022-12-22 2023 /pmc/articles/PMC10039835/ /pubmed/36547838 http://dx.doi.org/10.1007/s11356-022-24800-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Article
Hassan, Nancy Husseiny
Yousef, Doaa Mohammed
Alsemeh, Amira Ebrahim
Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title_full Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title_fullStr Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title_full_unstemmed Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title_short Hesperidin protects against aluminum-induced renal injury in rats via modulating MMP-9 and apoptosis: biochemical, histological, and ultrastructural study
title_sort hesperidin protects against aluminum-induced renal injury in rats via modulating mmp-9 and apoptosis: biochemical, histological, and ultrastructural study
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10039835/
https://www.ncbi.nlm.nih.gov/pubmed/36547838
http://dx.doi.org/10.1007/s11356-022-24800-0
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