Cox-2 Inhibition Protects against HypoxiaReoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression
المؤلفون المشاركون
Irwin, Michael G.
Li, Haobo
Pang, Lei
Cai, Yin
Tang, Eva Hoi Ching
Ma, Haichun
Yan, Dan
Kosuru, Ramoji
Xia, Zhengyuan
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-17، 17ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-10-04
دولة النشر
مصر
عدد الصفحات
17
التخصصات الرئيسية
الملخص EN
The present study explored the potential causal link between ischemia-driven cyclooxygenase-2 (COX-2) expression and enhanced apoptosis during myocardial ischemia/reperfusion (I/R) by using H9C2 cardiomyocytes and primary rat cardiomyocytes subjected to hypoxia/reoxygenation (H/R).
The results showed that H/R resulted in higher COX-2 expression than that of controls, which was prevented by pretreatment with Helenalin (NFκB specific inhibitor).
Furthermore, pretreatment with NS398 (COX-2 specific inhibitor) significantly attenuated H/R-induced cell injury [lower lactate dehydrogenase (LDH) leakage and enhanced cell viability] and apoptosis (higher Bcl2 expression and lower level of cleaved caspases-3 and TUNEL-positive cells) in cardiomyocytes.
The amelioration of posthypoxic apoptotic cell death was paralleled by significant attenuation of H/R-induced increases in proinflammatory cytokines [interleukin 6 (IL6) and tumor necrosis factor (TNFα)] and reactive oxygen species (ROS) production and by higher protein expression of phosphorylated Akt and inducible nitric oxide synthase (iNOS) and enhanced nitric oxide production.
Moreover, the application of LY294002 (Akt-specific inhibitor) or 1400W (iNOS-selective inhibitor) cancelled the cellular protective effects of NS398.
Findings from the current study suggest that activation of NFκB during cardiomyocyte H/R induces the expression of COX-2 and that higher COX-2 expression during H/R exacerbates cardiomyocyte H/R injury via mechanisms that involve cross talks among inflammation, ROS, and Akt/iNOS/NO signaling.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Pang, Lei& Cai, Yin& Tang, Eva Hoi Ching& Yan, Dan& Kosuru, Ramoji& Li, Haobo…[et al.]. 2016. Cox-2 Inhibition Protects against HypoxiaReoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-17.
https://search.emarefa.net/detail/BIM-1113813
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Pang, Lei…[et al.]. Cox-2 Inhibition Protects against HypoxiaReoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-17.
https://search.emarefa.net/detail/BIM-1113813
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Pang, Lei& Cai, Yin& Tang, Eva Hoi Ching& Yan, Dan& Kosuru, Ramoji& Li, Haobo…[et al.]. Cox-2 Inhibition Protects against HypoxiaReoxygenation-Induced Cardiomyocyte Apoptosis via Akt-Dependent Enhancement of iNOS Expression. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-17.
https://search.emarefa.net/detail/BIM-1113813
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1113813
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