Norepinephrine Induces Lung Microvascular Endothelial Cell Death by NADPH Oxidase-Dependent Activation of Caspase-3
المؤلفون المشاركون
Chignalia, Andreia Z.
Weinberg, Guy
Dull, Randal O.
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-02-12
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Norepinephrine (NE) is the naturally occurring adrenergic agonist that is released in response to hypotension, and it is routinely administered in clinical settings to treat moderate to severe hypotension that may occur during general anesthesia and shock states.
Although NE has incontestable beneficial effects on blood pressure maintenance during hypotensive conditions, deleterious effects of NE on endothelial cell function may occur.
In particular, the role of reactive oxygen species (ROS) and NADPH oxidase (Nox) on the deleterious effects of NE on endothelial cell function have not been fully elucidated.
Therefore, we investigated the effects of NE on ROS production in rat lung microvascular endothelial cells (RLMEC) and its contribution to cell death.
RLMEC were treated with NE (5 ng/mL) for 24 hours and ROS production was assessed by CellROX and DCFDA fluorescence.
Nox activity was assessed by NADPH-stimulated ROS production in isolated membranes and phosphorylation of p47phox; cell death was assessed by flow cytometry and DNA fragmentation.
Caspase activation was assessed by fluorescent microscopy.
Nox1, Nox2, and Nox4 mRNA expression was assessed by real-time PCR.
NE increased ROS production, Nox activity, p47phox phosphorylation, Nox2 and Nox4 mRNA content, caspase-3 activation, and RLMEC death.
Phentolamine, an α1-adrenoreceptor antagonist, inhibited NE-induced ROS production and Nox activity and partly inhibited cell death while β-blockade had no effect.
Apocynin and PEGSOD inhibited NE-induced caspase-3 activation and cell death while direct inhibition of caspase-3 abrogated NE-induced cell death.
PEG-CAT inhibited NE-induced cell death but not caspase-3 activation.
Collectively, these results indicate that NE induces RLMEC death via activation of Nox by α-adrenergic signaling and caspase-3-dependent pathways.
NE has deleterious effects on RLMECs that may be important to its long-term therapeutic use.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chignalia, Andreia Z.& Weinberg, Guy& Dull, Randal O.. 2020. Norepinephrine Induces Lung Microvascular Endothelial Cell Death by NADPH Oxidase-Dependent Activation of Caspase-3. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-11.
https://search.emarefa.net/detail/BIM-1203998
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chignalia, Andreia Z.…[et al.]. Norepinephrine Induces Lung Microvascular Endothelial Cell Death by NADPH Oxidase-Dependent Activation of Caspase-3. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-11.
https://search.emarefa.net/detail/BIM-1203998
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chignalia, Andreia Z.& Weinberg, Guy& Dull, Randal O.. Norepinephrine Induces Lung Microvascular Endothelial Cell Death by NADPH Oxidase-Dependent Activation of Caspase-3. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-11.
https://search.emarefa.net/detail/BIM-1203998
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203998
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