Dexmedetomidine Alleviates Propofol Infusion Syndrome-Induced Myocardial Injury through Inhibiting Ferroptosis Associated with Accumulation of Reactive Oxygen Species
© 2024 by the Association of Clinical Scientists, Inc..
OBJECTIVE: To observe the effect of dexmedetomidine (Dex) on propofol infusion syndrome (PRIS)-induced myocardial injury and explore the roles of ferroptosis and accumulation of reactive oxygen species (ROS).
METHODS: Eighteen male Sprague-Dawley rats were evenly divided into the control group, model group and test group (n=6/group) based on a computer-generated random number table. The PRIS-induced myocardial injury model was prepared in the model group and test group through a 12 h-caudal vein infusion of 1% propofol medium and long chain fat emulsion injection at a rate of 20 mg·Kg-1·h-1 for the first 6 h and 40 mg·Kg-1·h--1 for the last 6 h, and meanwhile the test group was treated by Dex. The control group received the same amount of normal saline through the caudal vein. The following indicators were compared between the three groups including myocardial pathological results, enzymatic changes of myocardial injury, ferroptosis of myocardial cells and accumulation of ROS.
RESULTS: Dex alleviated the myocardial pathological injury caused by propofol infusion. Propofol infusion caused time-dependent enzymatic changes of myocardial injury and Dex alleviated these enzymatic changes. Dex alleviated the ferroptosis of myocardial cells and accumulation of ROS caused by propofol infusion.
CONCLUSIONS: Dex could alleviate PRIS-induced myocardial injury by inhibiting ferroptosis associated with accumulation of ROS. Combined sedation using propofol and Dex might be a potential strategy for the prevention and treatment of PRIS-induced cardiotoxicity.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:54 |
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| Enthalten in: |
Annals of clinical and laboratory science - 54(2024), 1 vom: 21. Jan., Seite 86-91 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Sun, Jinhui [VerfasserIn] |
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| Themen: |
67VB76HONO |
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| Anmerkungen: |
Date Completed 25.03.2024 Date Revised 25.03.2024 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM370036387 |
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| 100 | 1 | |a Sun, Jinhui |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Dexmedetomidine Alleviates Propofol Infusion Syndrome-Induced Myocardial Injury through Inhibiting Ferroptosis Associated with Accumulation of Reactive Oxygen Species |
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| 500 | |a Date Completed 25.03.2024 | ||
| 500 | |a Date Revised 25.03.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2024 by the Association of Clinical Scientists, Inc. | ||
| 520 | |a OBJECTIVE: To observe the effect of dexmedetomidine (Dex) on propofol infusion syndrome (PRIS)-induced myocardial injury and explore the roles of ferroptosis and accumulation of reactive oxygen species (ROS) | ||
| 520 | |a METHODS: Eighteen male Sprague-Dawley rats were evenly divided into the control group, model group and test group (n=6/group) based on a computer-generated random number table. The PRIS-induced myocardial injury model was prepared in the model group and test group through a 12 h-caudal vein infusion of 1% propofol medium and long chain fat emulsion injection at a rate of 20 mg·Kg-1·h-1 for the first 6 h and 40 mg·Kg-1·h--1 for the last 6 h, and meanwhile the test group was treated by Dex. The control group received the same amount of normal saline through the caudal vein. The following indicators were compared between the three groups including myocardial pathological results, enzymatic changes of myocardial injury, ferroptosis of myocardial cells and accumulation of ROS | ||
| 520 | |a RESULTS: Dex alleviated the myocardial pathological injury caused by propofol infusion. Propofol infusion caused time-dependent enzymatic changes of myocardial injury and Dex alleviated these enzymatic changes. Dex alleviated the ferroptosis of myocardial cells and accumulation of ROS caused by propofol infusion | ||
| 520 | |a CONCLUSIONS: Dex could alleviate PRIS-induced myocardial injury by inhibiting ferroptosis associated with accumulation of ROS. Combined sedation using propofol and Dex might be a potential strategy for the prevention and treatment of PRIS-induced cardiotoxicity | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Dexmedetomidine | |
| 650 | 4 | |a Ferroptosis | |
| 650 | 4 | |a Myocardial injury | |
| 650 | 4 | |a Propofol infusion syndrome | |
| 650 | 4 | |a Reactive oxygen species | |
| 650 | 7 | |a Propofol |2 NLM | |
| 650 | 7 | |a YI7VU623SF |2 NLM | |
| 650 | 7 | |a Dexmedetomidine |2 NLM | |
| 650 | 7 | |a 67VB76HONO |2 NLM | |
| 650 | 7 | |a Reactive Oxygen Species |2 NLM | |
| 700 | 1 | |a Zhang, Bing |e verfasserin |4 aut | |
| 700 | 1 | |a Geng, Qiang |e verfasserin |4 aut | |
| 700 | 1 | |a Halimujiang, Jiayinati |e verfasserin |4 aut | |
| 700 | 1 | |a Song, Chang |e verfasserin |4 aut | |
| 700 | 1 | |a Xi, Min |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Ting |e verfasserin |4 aut | |
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