Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation
المؤلفون المشاركون
Kwak, Young-Lan
Jun, Ji Hae
Shim, Jae-Kwang
Oh, Ju Eun
Shin, Eun-Jung
Shin, Eunah
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-8، 8ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-01-09
دولة النشر
مصر
عدد الصفحات
8
التخصصات الرئيسية
الملخص EN
Emerging evidence indicates the pronounced role of inflammasome activation linked to reactive oxygen species (ROS) in the sterile inflammatory response triggered by ischemia/reperfusion (I/R) injury.
Ethyl pyruvate (EP) is an antioxidant and conveys myocardial protection against I/R injury, while the exact mechanisms remain elusive.
We aimed to investigate the effect of EP on myocardial I/R injury through mechanisms related to ROS and inflammasome regulation.
The rats were randomly assigned to four groups: (1) sham, (2) I/R-control (IRC), (3) EP-pretreatment + I/R, and (4) I/R + EP-posttreatment.
I/R was induced by a 30 min ligation of the left anterior descending artery followed by 4 h of reperfusion.
EP (50 mg/kg) was administered intraperitoneally at 1 h before ischemia (pretreatment) or upon reperfusion (posttreatment).
Both pre- and post-EP treatment resulted in significant reductions in myocardial infarct size (by 34% and 31%, respectively) and neutrophil infiltration.
I/R-induced myocardial expressions of NADPH oxidase-4, carnitine palmitoyltransferase 1A, and thioredoxin-interacting protein (TXNIP) were mitigated by EP.
EP treatment was associated with diminished inflammasome activation (NOD-like receptor 3 (NLRP3), apoptosis-associated speck-like protein, and caspase-1) and interleukin-1β induced by I/R.
I/R-induced phosphorylation of ERK and p38 were also mitigated with EP treatments.
In H9c2 cells, hypoxia-induced TXNIP and NLRP3 expressions were inhibited by EP and to a lesser degree by U0126 (MEK inhibitor) and SB203580 (p38 inhibitor) as well.
EP’s downstream protective mechanisms in myocardial I/R injury would include mitigation of ROS-mediated NLRP3 inflammasome upregulation and its associated pathways, partly via inhibition of hypoxia-induced phosphorylation of ERK and p38.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Jun, Ji Hae& Shim, Jae-Kwang& Oh, Ju Eun& Shin, Eun-Jung& Shin, Eunah& Kwak, Young-Lan. 2019. Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-8.
https://search.emarefa.net/detail/BIM-1203540
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Jun, Ji Hae…[et al.]. Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-8.
https://search.emarefa.net/detail/BIM-1203540
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Jun, Ji Hae& Shim, Jae-Kwang& Oh, Ju Eun& Shin, Eun-Jung& Shin, Eunah& Kwak, Young-Lan. Protective Effect of Ethyl Pyruvate against Myocardial Ischemia Reperfusion Injury through Regulations of ROS-Related NLRP3 Inflammasome Activation. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-8.
https://search.emarefa.net/detail/BIM-1203540
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203540
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