Soluble Receptor for Advanced Glycation End Product Ameliorates Chronic Intermittent Hypoxia Induced Renal Injury, Inflammation, and Apoptosis via P38JNK Signaling Pathways
المؤلفون المشاركون
Li, Shanqun
Wu, Xu
Gu, Wenyu
Lu, Huan
Liu, Chengying
Yu, Biyun
Xu, Hui
Tang, Yaodong
Zhou, Jian
Shao, Chuan
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-09-05
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Obstructive sleep apnea (OSA) associated chronic kidney disease is mainly caused by chronic intermittent hypoxia (CIH) triggered tissue damage.
Receptor for advanced glycation end product (RAGE) and its ligand high mobility group box 1 (HMGB1) are expressed on renal cells and mediate inflammatory responses in OSA-related diseases.
To determine their roles in CIH-induced renal injury, soluble RAGE (sRAGE), the RAGE neutralizing antibody, was intravenously administered in a CIH model.
We also evaluated the effect of sRAGE on inflammation and apoptosis.
Rats were divided into four groups: (1) normal air (NA), (2) CIH, (3) CIH+sRAGE, and (4) NA+sRAGE.
Our results showed that CIH accelerated renal histological injury and upregulated RAGE-HMGB1 levels involving inflammatory (NF-κB, TNF-α, and IL-6), apoptotic (Bcl-2/Bax), and mitogen-activated protein kinases (phosphorylation of P38, ERK, and JNK) signal transduction pathways, which were abolished by sRAGE but p-ERK.
Furthermore, sRAGE ameliorated renal dysfunction by attenuating tubular endothelial apoptosis determined by immunofluorescence staining of CD31 and TUNEL.
These findings suggested that RAGE-HMGB1 activated chronic inflammatory transduction cascades that contributed to the pathogenesis of the CIH-induced renal injury.
Inhibition of RAGE ligand interaction by sRAGE provided a therapeutic potential for CIH-induced renal injury, inflammation, and apoptosis through P38 and JNK pathways.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Wu, Xu& Gu, Wenyu& Lu, Huan& Liu, Chengying& Yu, Biyun& Xu, Hui…[et al.]. 2016. Soluble Receptor for Advanced Glycation End Product Ameliorates Chronic Intermittent Hypoxia Induced Renal Injury, Inflammation, and Apoptosis via P38JNK Signaling Pathways. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-13.
https://search.emarefa.net/detail/BIM-1113582
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Wu, Xu…[et al.]. Soluble Receptor for Advanced Glycation End Product Ameliorates Chronic Intermittent Hypoxia Induced Renal Injury, Inflammation, and Apoptosis via P38JNK Signaling Pathways. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-13.
https://search.emarefa.net/detail/BIM-1113582
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Wu, Xu& Gu, Wenyu& Lu, Huan& Liu, Chengying& Yu, Biyun& Xu, Hui…[et al.]. Soluble Receptor for Advanced Glycation End Product Ameliorates Chronic Intermittent Hypoxia Induced Renal Injury, Inflammation, and Apoptosis via P38JNK Signaling Pathways. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-13.
https://search.emarefa.net/detail/BIM-1113582
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1113582
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