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Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant
Coptisine (Cop) exerts a neuroprotective effect on central nervous system disease, particularly ischemic stroke. However, its protective mechanism is still unclear. This study aimed to investigate the protective effect of Cop on cerebral ischemia–reperfusion (IR) rats with a middle cerebral artery o...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10489949/ https://www.ncbi.nlm.nih.gov/pubmed/37687175 http://dx.doi.org/10.3390/molecules28176350 |
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author | Zhang, Junjie Qi, Ao Liu, Lulu Cai, Chun Xu, Hui |
author_facet | Zhang, Junjie Qi, Ao Liu, Lulu Cai, Chun Xu, Hui |
author_sort | Zhang, Junjie |
collection | PubMed |
description | Coptisine (Cop) exerts a neuroprotective effect on central nervous system disease, particularly ischemic stroke. However, its protective mechanism is still unclear. This study aimed to investigate the protective effect of Cop on cerebral ischemia–reperfusion (IR) rats with a middle cerebral artery occlusion model by integrating a gas chromatography–mass spectrometry (GC–MS)-based metabolomics approach with biochemical assessment. Our results showed that Cop could improve neurobehavioral function and decrease the ischemia size in IR rats. In addition, Cop was found to decrease inflammatory mediators (e.g., prostaglandin D2 (PGD2) and tumor necrosis factor-α (TNF-α) and attenuate oxidative stress response (e.g., increase the superoxide dismutase (SOD) expression and decrease 8-iso-PGF2α level). Furthermore, the GC-MS-based cerebrospinal fluid (CSF) metabolomics analysis indicated that Cop influenced the level of glycine, 2,3,4-trihydroxybutyric acid, oleic acid, glycerol, and ribose during IR injury. Cop exhibited a good neuroprotective effect against cerebral IR injury and metabolic alterations, which might be mediated through its antioxidant and anti-inflammatory properties. |
format | Online Article Text |
id | pubmed-10489949 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-104899492023-09-09 Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant Zhang, Junjie Qi, Ao Liu, Lulu Cai, Chun Xu, Hui Molecules Article Coptisine (Cop) exerts a neuroprotective effect on central nervous system disease, particularly ischemic stroke. However, its protective mechanism is still unclear. This study aimed to investigate the protective effect of Cop on cerebral ischemia–reperfusion (IR) rats with a middle cerebral artery occlusion model by integrating a gas chromatography–mass spectrometry (GC–MS)-based metabolomics approach with biochemical assessment. Our results showed that Cop could improve neurobehavioral function and decrease the ischemia size in IR rats. In addition, Cop was found to decrease inflammatory mediators (e.g., prostaglandin D2 (PGD2) and tumor necrosis factor-α (TNF-α) and attenuate oxidative stress response (e.g., increase the superoxide dismutase (SOD) expression and decrease 8-iso-PGF2α level). Furthermore, the GC-MS-based cerebrospinal fluid (CSF) metabolomics analysis indicated that Cop influenced the level of glycine, 2,3,4-trihydroxybutyric acid, oleic acid, glycerol, and ribose during IR injury. Cop exhibited a good neuroprotective effect against cerebral IR injury and metabolic alterations, which might be mediated through its antioxidant and anti-inflammatory properties. MDPI 2023-08-30 /pmc/articles/PMC10489949/ /pubmed/37687175 http://dx.doi.org/10.3390/molecules28176350 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Zhang, Junjie Qi, Ao Liu, Lulu Cai, Chun Xu, Hui Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title | Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title_full | Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title_fullStr | Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title_full_unstemmed | Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title_short | Gas Chromatography–Mass Spectrometry-Based Cerebrospinal Fluid Metabolomics to Reveal the Protection of Coptisine against Transient Focal Cerebral Ischemia–Reperfusion Injury via Anti-Inflammation and Antioxidant |
title_sort | gas chromatography–mass spectrometry-based cerebrospinal fluid metabolomics to reveal the protection of coptisine against transient focal cerebral ischemia–reperfusion injury via anti-inflammation and antioxidant |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10489949/ https://www.ncbi.nlm.nih.gov/pubmed/37687175 http://dx.doi.org/10.3390/molecules28176350 |
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