دورية أكاديمية
Inhibition of Extracellular Signal-Regulated Kinase Activity Improves Cognitive Function in Mice Subjected to Myocardial Infarction.
| العنوان: | Inhibition of Extracellular Signal-Regulated Kinase Activity Improves Cognitive Function in Mice Subjected to Myocardial Infarction. |
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| المؤلفون: | Yin Y; Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, School of Medicine, No. 241 West Huaihai Rd., Shanghai, China., Li X; School of Medical Instrument and Food Engineering USST, University of Shanghai for Science and Technology, Shanghai, China., Zhang X; School of Medicine, Shanghai University, No. 99 Shangda Road, Baoshan District, Shanghai, 200444, China., Yuan X; School of Medicine, Shanghai University, No. 99 Shangda Road, Baoshan District, Shanghai, 200444, China., You X; School of Medicine, Shanghai University, No. 99 Shangda Road, Baoshan District, Shanghai, 200444, China. yoyo1976@shu.edu.cn., Wu J; Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, School of Medicine, No. 241 West Huaihai Rd., Shanghai, China. wu_jingxiang@sjtu.edu.cn.; School of Medical Instrument and Food Engineering USST, University of Shanghai for Science and Technology, Shanghai, China. wu_jingxiang@sjtu.edu.cn. |
| المصدر: | Cardiovascular toxicology [Cardiovasc Toxicol] 2024 Aug; Vol. 24 (8), pp. 766-775. Date of Electronic Publication: 2024 Jun 08. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Humana Press Country of Publication: United States NLM ID: 101135818 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1559-0259 (Electronic) Linking ISSN: 15307905 NLM ISO Abbreviation: Cardiovasc Toxicol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Totowa, NJ : Humana Press, c2001- |
| مواضيع طبية MeSH: | Myocardial Infarction*/enzymology , Myocardial Infarction*/physiopathology , Myocardial Infarction*/pathology , Myocardial Infarction*/drug therapy , Cognition*/drug effects , Nitriles*/pharmacology , Disease Models, Animal* , Butadienes*/pharmacology , Extracellular Signal-Regulated MAP Kinases*/metabolism , Extracellular Signal-Regulated MAP Kinases*/antagonists & inhibitors , Behavior, Animal*/drug effects , Mice, Inbred C57BL* , STAT1 Transcription Factor*/metabolism , STAT1 Transcription Factor*/antagonists & inhibitors, Animals ; Male ; Protein Kinase Inhibitors/pharmacology ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/physiopathology ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/enzymology ; Cognitive Dysfunction/prevention & control ; Signal Transduction/drug effects ; Elevated Plus Maze Test ; Open Field Test/drug effects ; Mice |
| مستخلص: | Cognitive impairment is a commonly observed complication following myocardial infarction; however, the underlying mechanisms are still not well understood. The most recent research suggests that extracellular signal-regulated kinase (ERK) plays a critical role in the development and occurrence of cognitive dysfunction-related diseases. This study aims to explore whether the ERK inhibitor U0126 targets the ERK/Signal Transducer and Activator of Transcription 1 (STAT1) pathway to ameliorate cognitive impairment after myocardial infarction. To establish a mouse model of myocardial infarction, we utilized various techniques including Echocardiography, Hematoxylin-eosin (HE) staining, Elisa, Open field test, Elevated plus maze test, and Western blot analysis to assess mouse cardiac function, cognitive function, and signal transduction pathways. For further investigation into the mechanisms of cognitive function and signal transduction, we administered the ERK inhibitor U0126 via intraperitoneal injection. Reduced total distance and activity range were observed in mice subjected to myocardial infarction during the open field test, along with decreased exploration of the open arms in the elevated plus maze test. However, U0126 treatment exhibited a significant improvement in cognitive decline, indicating a protective effect through the inhibition of the ERK/STAT1 signaling pathway. Hence, this study highlights the involvement of the ERK/STAT1 pathway in regulating cognitive dysfunction following myocardial infarction and establishes U0126 as a promising therapeutic target. (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.) |
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| معلومات مُعتمدة: | 82071233 National Natural Science Foundation of China; SHDC2020CR4063 Shanghai Shen Kang Hospital Development Center Project |
| فهرسة مساهمة: | Keywords: Animal model; Behavioral experiment; Cardiovascular disease; Extracesllular signal-regulated kinase; U0126 |
| المشرفين على المادة: | 0 (U 0126) 0 (Nitriles) 0 (Butadienes) EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases) 0 (STAT1 Transcription Factor) 0 (Stat1 protein, mouse) 0 (Protein Kinase Inhibitors) |
| تواريخ الأحداث: | Date Created: 20240608 Date Completed: 20240805 Latest Revision: 20240805 |
| رمز التحديث: | 20240806 |
| DOI: | 10.1007/s12012-024-09877-y |
| PMID: | 38850470 |
| قاعدة البيانات: | MEDLINE |
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Full Text Finder | تدمد: | 1559-0259 |
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| DOI: | 10.1007/s12012-024-09877-y |