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Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways
المؤلفون المشاركون
Xu, Jian
Li, Xiang
He, Mengyu
Zhu, Jiali
Kong, Hui
Xie, Weiping
Shi, Wen
Yu, Min
Jin, Linling
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-03-10
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Acute lung injury (ALI) is a devastating critical disease characterized by diffuse inflammation and endothelial dysfunction.
Increasing evidence, including from our laboratory, has revealed that the opening of ATP-sensitive potassium (KATP) channels has promising anti-inflammation and endothelial protection activities in various disorders.
However, the impacts of KATP channels on ALI remain obscure.
In this study, we used nicorandil (Nico), a classic KATP channel opener, to investigate whether opening of KATP channels could alleviate ALI with an emphasis on human pulmonary artery endothelial cell (HPAEC) modulation.
The results showed that Nico inhibited lipopolysaccharide- (LPS-) induced inflammatory response, protein accumulation, myeloperoxidase activity, and endothelial injury.
In vitro, Nico reduced LPS-induced HPAEC apoptosis and the expression of cleaved-caspase-3, caspase-9, and CCAAT/enhancer-binding protein homologous protein (CHOP).
Additionally, Nico inhibited inflammation by suppressing monocyte-endothelial adhesion and decreasing the expression of proinflammatory proteins.
Moreover, Nico restored the expression and the distribution of adherens junction vascular endothelial- (VE-) cadherin.
Further, Nico abolished the increase in intracellular reactive oxygen species (ROS) and the activation of NF-κB and mitogen-activated protein kinase (MAPK) in HPAECs.
Glibenclamide (Gli), a nonselective KATP channel blocker, abrogated the effects of Nico, implying that opening of KATP channels contributes to the relief of ALI.
Together, our findings indicated that Nico alleviated LPS-induced ALI by protecting ECs function via preventing apoptosis, suppressing endothelial inflammation and reducing oxidative stress, which may be attributed to the inhibition of NF-κB and MAPK signaling pathways.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
He, Mengyu& Shi, Wen& Yu, Min& Li, Xiang& Xu, Jian& Zhu, Jiali…[et al.]. 2019. Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1203887
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
He, Mengyu…[et al.]. Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1203887
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
He, Mengyu& Shi, Wen& Yu, Min& Li, Xiang& Xu, Jian& Zhu, Jiali…[et al.]. Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1203887
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1203887
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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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
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