Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROSJNK Signaling Pathway
المؤلفون المشاركون
Hu, Xueyuan
Chen, Yongping
Feng, Xiujing
Sha, Jichen
Li, Bei
Zhang, Huayun
Fan, Honggang
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-09-03
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Acute stress induces tissue damage through excessive oxidative stress.
Dexmedetomidine (DEX) reportedly has an antioxidant effect.
However, protective roles and related potential molecular mechanisms of DEX against kidney injury induced by acute stress are unknown.
Herein, rats were forced to swim 15 min followed by restraint stress for 3 h with/without DEX (30 μg/kg).
Successful model establishment was validated by an open-field test.
Assessment of renal function (creatinine, urea nitrogen), histopathology, oxidative stress (malondialdehyde, glutathione, and superoxide dismutase), and apoptosis (transferase-mediated dUTP nick end labeling) was performed.
Localization of apoptosis was determined by immunohistochemistry of cleaved caspase 3 protein.
In addition, key proteins of the death receptor-mediated pathway, mitochondrial pathway, endoplasmic reticulum stress (ERS) pathway, and ROS/JNK signaling pathway were measured by Western blot.
We found that DEX significantly improved renal dysfunction, ameliorated kidney injury, reduced oxidative stress, and alleviated apoptosis.
DEX also inhibited the release of norepinephrine (NE), decreased the production of reactive oxygen species (ROS), and inhibited JNK phosphorylation.
Additionally, DEX downregulated the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3 proteins in mitochondria-dependent pathways.
In summary, DEX protects against acute stress-induced kidney injury in rats by reducing oxidative stress and apoptosis via inhibition of the ROS/JNK pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chen, Yongping& Feng, Xiujing& Hu, Xueyuan& Sha, Jichen& Li, Bei& Zhang, Huayun…[et al.]. 2018. Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROSJNK Signaling Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1211347
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chen, Yongping…[et al.]. Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROSJNK Signaling Pathway. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-12.
https://search.emarefa.net/detail/BIM-1211347
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chen, Yongping& Feng, Xiujing& Hu, Xueyuan& Sha, Jichen& Li, Bei& Zhang, Huayun…[et al.]. Dexmedetomidine Ameliorates Acute Stress-Induced Kidney Injury by Attenuating Oxidative Stress and Apoptosis through Inhibition of the ROSJNK Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1211347
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1211347
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