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Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway
المؤلفون المشاركون
Gao, Wei
Gong, Jing
Tai, Qi-Hang
Xu, Guang-Xiao
Wang, Xue-Ting
Zhu, Jing-Li
Zhao, Xiao-Qing
Sun, Hai-Bin
Zhu, Dan
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-08-18
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Background.
Brain injury is the leading cause of death following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR).
Ac2-26 and endothelial nitric oxide synthase (eNOS) have been shown to reduce neuroinflammation.
This study is aimed at determining the mechanism by which Ac2-26 protects against inflammation during brain injury following CA and CPR.
Methods.
Sixty-four rats were randomized into sham, saline, Ac2-26, and Ac2-26+L-NIO (endothelial nitric oxide synthase (eNOS) inhibitor) groups.
Rats received Ac2-26, Ac2-26+L-NIO, or saline after CPR.
Neurologic function was assessed at baseline, 24, and 72 hours after CPR.
At 72 hours after resuscitation, serum and brain tissues were collected.
Results.
Blood-brain barrier (BBB) permeability increased, and the number of surviving neurons and neurological function decreased in the saline group compared to the sham group.
Anti-inflammatory and proinflammatory factors, neuron-specific enolase (NSE) levels, and the expression of eNOS, phosphorylated (p)-eNOS, inducible nitric oxide synthase (iNOS), and oxidative stress-related factors in the three CA groups significantly increased (P<0.05).
BBB permeability decreased, and the number of surviving neurons and neurological function increased in the Ac2-26 group compared to the saline group (P<0.05).
Ac2-26 increased anti-inflammatory and reduced proinflammatory markers, raised NSE levels, increased the expression of eNOS and p-eNOS, and reduced the expression of iNOS and oxidative stress-related factors compared to the saline group (P<0.05).
The effect of Ac2-26 on brain injury was reversed by L-NIO (P<0.05).
Conclusions.
Ac2-26 reduced brain injury after CPR by inhibiting oxidative stress and neuroinflammation and protecting the BBB.
The therapeutic effect of Ac2-26 on brain injury was largely dependent on the eNOS pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Gong, Jing& Tai, Qi-Hang& Xu, Guang-Xiao& Wang, Xue-Ting& Zhu, Jing-Li& Zhao, Xiao-Qing…[et al.]. 2020. Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway. Mediators of Inflammation،Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1191689
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Gong, Jing…[et al.]. Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway. Mediators of Inflammation No. 2020 (2020), pp.1-10.
https://search.emarefa.net/detail/BIM-1191689
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Gong, Jing& Tai, Qi-Hang& Xu, Guang-Xiao& Wang, Xue-Ting& Zhu, Jing-Li& Zhao, Xiao-Qing…[et al.]. Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway. Mediators of Inflammation. 2020. Vol. 2020, no. 2020, pp.1-10.
https://search.emarefa.net/detail/BIM-1191689
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1191689
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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