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In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury
Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of Gram-negative bacteria, which induces multiple organ dysfunctions, eventually leading to septic shock and death. Arjunolic acid (AA) has been shown to have therapeutic benefits against various organ pathophysiologies, although it...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857905/ https://www.ncbi.nlm.nih.gov/pubmed/35190789 http://dx.doi.org/10.7717/peerj.12986 |
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author | Elsawy, Hany Almalki, Mohammed Elmenshawy, Omar Abdel-Moneim, Ashraf |
author_facet | Elsawy, Hany Almalki, Mohammed Elmenshawy, Omar Abdel-Moneim, Ashraf |
author_sort | Elsawy, Hany |
collection | PubMed |
description | Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of Gram-negative bacteria, which induces multiple organ dysfunctions, eventually leading to septic shock and death. Arjunolic acid (AA) has been shown to have therapeutic benefits against various organ pathophysiologies, although its role in sepsis remains unclear. Here, we evaluated the effects of AA on LPS-induced free radical production and cardiotoxicity. Male albino mice were allocated to four groups: normal, 1.5 µg/30 g b.w. of LPS (LPS), 20 mg/kg b.w. AA with LPS (AA+LPS) and 20 mg/kg b.w. of AA (AA). Subsequently, blood and heart samples were harvested for biochemical and histopathological examinations. Pretreatment with AA attenuated LPS-induced increased serum levels of cardiac troponin I, lactate dehydrogenase and creatine kinase. In the meantime, AA pretreatment before LPS resulted in a significant increase in endogenous antioxidants (superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione) and a significant decrease in the level of lipid peroxidation product (malondialdehyde) in the heart as compared to the LPS group, while cardiac cytochrome c activity were significantly increased. In addition, in the AA-pretreated mice, C-reactive protein and proinflammatory cytokines (interlukin-1 and tumor necrosis factor-alpha) were significantly reduced, and anti-inflammatory cytokines (interleukin-4 and -10) were significantly increased in cardiac tissues as compared to the LPS-treated animals. Furthermore, prior administration of AA to LPS exposed mice led to a significant a significant decrease in heart caspase-3, -8, and -9 as compared to the LPS group. Interestingly, AA was also able to improve LPS-induced histopathological changes in the cardiomyocytes. In conclusion, these in vivo findings indicate that AA may be a promising cardioprotective agent against LPS-stimulated cardiotoxicity, at least in part, through upregulation of cardiac antioxidants, reduction of lipid peroxidation, and inhibition of inflammation and cardiac cell death. |
format | Online Article Text |
id | pubmed-8857905 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-88579052022-02-20 In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury Elsawy, Hany Almalki, Mohammed Elmenshawy, Omar Abdel-Moneim, Ashraf PeerJ Biochemistry Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of Gram-negative bacteria, which induces multiple organ dysfunctions, eventually leading to septic shock and death. Arjunolic acid (AA) has been shown to have therapeutic benefits against various organ pathophysiologies, although its role in sepsis remains unclear. Here, we evaluated the effects of AA on LPS-induced free radical production and cardiotoxicity. Male albino mice were allocated to four groups: normal, 1.5 µg/30 g b.w. of LPS (LPS), 20 mg/kg b.w. AA with LPS (AA+LPS) and 20 mg/kg b.w. of AA (AA). Subsequently, blood and heart samples were harvested for biochemical and histopathological examinations. Pretreatment with AA attenuated LPS-induced increased serum levels of cardiac troponin I, lactate dehydrogenase and creatine kinase. In the meantime, AA pretreatment before LPS resulted in a significant increase in endogenous antioxidants (superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione) and a significant decrease in the level of lipid peroxidation product (malondialdehyde) in the heart as compared to the LPS group, while cardiac cytochrome c activity were significantly increased. In addition, in the AA-pretreated mice, C-reactive protein and proinflammatory cytokines (interlukin-1 and tumor necrosis factor-alpha) were significantly reduced, and anti-inflammatory cytokines (interleukin-4 and -10) were significantly increased in cardiac tissues as compared to the LPS-treated animals. Furthermore, prior administration of AA to LPS exposed mice led to a significant a significant decrease in heart caspase-3, -8, and -9 as compared to the LPS group. Interestingly, AA was also able to improve LPS-induced histopathological changes in the cardiomyocytes. In conclusion, these in vivo findings indicate that AA may be a promising cardioprotective agent against LPS-stimulated cardiotoxicity, at least in part, through upregulation of cardiac antioxidants, reduction of lipid peroxidation, and inhibition of inflammation and cardiac cell death. PeerJ Inc. 2022-02-16 /pmc/articles/PMC8857905/ /pubmed/35190789 http://dx.doi.org/10.7717/peerj.12986 Text en ©2022 Elsawy et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited. |
spellingShingle | Biochemistry Elsawy, Hany Almalki, Mohammed Elmenshawy, Omar Abdel-Moneim, Ashraf In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title | In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title_full | In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title_fullStr | In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title_full_unstemmed | In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title_short | In vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
title_sort | in vivo evaluation of the protective effects of arjunolic acid against lipopolysaccharide-induced septic myocardial injury |
topic | Biochemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857905/ https://www.ncbi.nlm.nih.gov/pubmed/35190789 http://dx.doi.org/10.7717/peerj.12986 |
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