Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction

Մատենագիտական մանրամասներ
Parent link:Biomedicines
Vol. 11, iss. 3.— 2023.— [714, 15 p.]
Համատեղ հեղինակ: Национальный исследовательский Томский политехнический университет Инженерная школа новых производственных технологий Научно-образовательный центр Н. М. Кижнера
Այլ հեղինակներ: Plotnikov M. B. Mark, Chernysheva G. A. Galina, Smol'yakova V. I. Vera, Aliev O. I. Oleg, Fomina T. I. Tatyana, Sandrikina L. A. Lyubov, Sukhodolo I. V. Irina, Ivanova V. V. Vera, Osipenko A. N. Anton, Anfinogenova N. D. Nina, Khlebnikov A. I. Andrey Ivanovich, Atochin D. N. Dmitry Nikolaevich, Schepetkin (Shchepyotkin) I. A. Igor Aleksandrovich, Quinn M. T. Mark
Ամփոփում:Title screen
Activation of c-Jun N-terminal kinases (JNKs) is involved in myocardial injury, left ventricular remodeling (LV), and heart failure (HF) after myocardial infarction (MI). The aim of this research was to evaluate the effects of a selective JNK inhibitor, 11H-indeno [1,2-b]quinoxalin-11-one oxime (IQ-1), on myocardial injury and acute myocardial ischemia/reperfusion (I/R) in adult male Wistar rats. Intraperitoneal administration of IQ-1 (25 mg/kg daily for 5 days) resulted in a significant decrease in myocardial infarct size on day 5 after MI. On day 60 after MI, a significant (2.6-fold) decrease in LV scar size, a 2.2-fold decrease in the size of the LV cavity, a 2.9-fold decrease in the area of mature connective tissue, and a 1.7-fold decrease in connective tissue in the interventricular septum were observed compared with the control group. The improved contractile function of the heart resulted in a significant (33%) increase in stroke size, a 40% increase in cardiac output, a 12% increase in LV systolic pressure, a 28% increase in the LV maximum rate of pressure rise, a 45% increase in the LV maximum rate of pressure drop, a 29% increase in the contractility index, a 14% increase in aortic pressure, a 2.7-fold decrease in LV end-diastolic pressure, and a 4.2-fold decrease in LV minimum pressure. We conclude that IQ-1 has cardioprotective activity and reduces the severity of HF after MI.
Լեզու:անգլերեն
Հրապարակվել է: 2023
Խորագրեր:
Առցանց հասանելիություն:http://earchive.tpu.ru/handle/11683/74886
https://doi.org/10.3390/biomedicines11030714
Ձևաչափ: Էլեկտրոնային Գրքի գլուխ
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=669249

MARC

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200 1 |a Cardioprotective Effects of a Selective c-Jun N-terminal Kinase Inhibitor in a Rat Model of Myocardial Infarction  |f M. B. Plotnikov, G. A. Chernysheva, V. I. Smol'yakova [et al.] 
203 |a Text  |c electronic 
300 |a Title screen 
320 |a [References: 92 tit.] 
330 |a Activation of c-Jun N-terminal kinases (JNKs) is involved in myocardial injury, left ventricular remodeling (LV), and heart failure (HF) after myocardial infarction (MI). The aim of this research was to evaluate the effects of a selective JNK inhibitor, 11H-indeno [1,2-b]quinoxalin-11-one oxime (IQ-1), on myocardial injury and acute myocardial ischemia/reperfusion (I/R) in adult male Wistar rats. Intraperitoneal administration of IQ-1 (25 mg/kg daily for 5 days) resulted in a significant decrease in myocardial infarct size on day 5 after MI. On day 60 after MI, a significant (2.6-fold) decrease in LV scar size, a 2.2-fold decrease in the size of the LV cavity, a 2.9-fold decrease in the area of mature connective tissue, and a 1.7-fold decrease in connective tissue in the interventricular septum were observed compared with the control group. The improved contractile function of the heart resulted in a significant (33%) increase in stroke size, a 40% increase in cardiac output, a 12% increase in LV systolic pressure, a 28% increase in the LV maximum rate of pressure rise, a 45% increase in the LV maximum rate of pressure drop, a 29% increase in the contractility index, a 14% increase in aortic pressure, a 2.7-fold decrease in LV end-diastolic pressure, and a 4.2-fold decrease in LV minimum pressure. We conclude that IQ-1 has cardioprotective activity and reduces the severity of HF after MI. 
461 |t Biomedicines 
463 |t Vol. 11, iss. 3  |v [714, 15 p.]  |d 2023 
610 1 |a электронный ресурс 
610 1 |a труды учёных ТПУ 
610 1 |a cardioprotective activity 
610 1 |a c-Jun N-terminal kinase inhibitor 
610 1 |a 11H-indeno[1,2-b]quinoxalin-11-one oxime 
610 1 |a heart failure 
610 1 |a infarct size 
610 1 |a myocardial infarction 
610 1 |a ischemia/reperfusion 
610 1 |a сердечная недостаточность 
610 1 |a инфаркт миокарда 
610 1 |a ишемия 
610 1 |a реперфузия 
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701 1 |a Anfinogenova  |b N. D.  |g Nina 
701 1 |a Khlebnikov  |b A. I.  |c Chemist  |c Professor of Tomsk Polytechnic University  |f 1963-  |g Andrey Ivanovich  |3 (RuTPU)RU\TPU\pers\33927  |9 17500 
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856 4 |u https://doi.org/10.3390/biomedicines11030714 
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