Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial IschemiaReperfusion Injury by Activation of RISK and Mitochondrial Pathways
المؤلفون المشاركون
Collino, Massimo
Pagliaro, Pasquale
Penna, Claudia
Tullio, Francesca
Femminò, Saveria
Serpe, Loredana
Collotta, Debora
Cocco, Mattia
Bertinaria, Massimo
Mastrocola, Raffaella
Nigro, Debora
Chiazza, Fausto
Aragno, Manuela
Alloatti, Giuseppe
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-12-08
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Although the nucleotide-binding oligomerization domain- (NOD-) like receptor pyrin domain containing 3 (NLRP3) inflammasome has been recently detected in the heart, its role in cardiac ischemia/reperfusion (IR) is still controversial.
Here, we investigate whether a pharmacological modulation of NLRP3 inflammasome exerted protective effects in an ex vivo model of IR injury.
Isolated hearts from male Wistar rats (5-6 months old) underwent ischemia (30 min) followed by reperfusion (20 or 60 min) with and without pretreatment with the recently synthetized NLRP3 inflammasome inhibitor INF4E (50 μM, 20 min before ischemia).
INF4E exerted protection against myocardial IR, shown by a significant reduction in infarct size and lactate dehydrogenase release and improvement in postischemic left ventricular pressure.
The formation of the NLRP3 inflammasome complex was induced by myocardial IR and attenuated by INF4E in a time-dependent way.
Interestingly, the hearts of the INF4E-pretreated animals displayed a marked improvement of the protective RISK pathway and this effect was associated increase in expression of markers of mitochondrial oxidative phosphorylation.
Our results demonstrate for the first time that INF4E protected against the IR-induced myocardial injury and dysfunction, by a mechanism that involves inhibition of the NLRP3 inflammasome, resulting in the activation of the prosurvival RISK pathway and improvement in mitochondrial function.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Mastrocola, Raffaella& Penna, Claudia& Tullio, Francesca& Femminò, Saveria& Nigro, Debora& Chiazza, Fausto…[et al.]. 2016. Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial IschemiaReperfusion Injury by Activation of RISK and Mitochondrial Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1114000
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Mastrocola, Raffaella…[et al.]. Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial IschemiaReperfusion Injury by Activation of RISK and Mitochondrial Pathways. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-11.
https://search.emarefa.net/detail/BIM-1114000
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Mastrocola, Raffaella& Penna, Claudia& Tullio, Francesca& Femminò, Saveria& Nigro, Debora& Chiazza, Fausto…[et al.]. Pharmacological Inhibition of NLRP3 Inflammasome Attenuates Myocardial IschemiaReperfusion Injury by Activation of RISK and Mitochondrial Pathways. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1114000
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1114000
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر