AT1RGSK-3βmTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo
المؤلفون المشاركون
Liu, Jiapeng
Si, Wei
Lenahan, Cameron
Li, Shirong
Wang, Lu
Wang, Qian
Li, Banghui
Gu, Ran
Qu, Hao
XikeWang, Qian
Hu, Xiao
Zuo, Gang
Tian, Tian
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-12-23
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Objective.
The focus of the present study is to evaluate the effects of Angiotensin II (Ang II) on neuronal apoptosis after HIE and the potential underlying mechanisms.
Methods.
Primary neonatal rat cortical neurons were used to study the oxygen-glucose deprivation (OGD) cell model.
The expressions of Ang II, AT1R, GSK-3β, p-GSK-3β, mTOR, p-mTOR, Bax, Bcl-2, and cleaved caspase-3 were detected via western blot.
IF and flow cytometry were used to evaluate neuronal apoptosis.
Hypoxic-ischemic encephalopathy (HIE) was established to evaluate the therapeutic effects of Ang II in vivo.
Cerebral infarction areas were detected by 2,3,5-Triphenyltetrazolium chloride staining.
The righting and geotaxis reflexes were also recorded.
In addition, Fluoro-Jade C staining and TUNEL staining were performed to evaluate neuronal degeneration and apoptosis.
Results.
Ang II significantly increased the rate of neuronal apoptosis, upregulated the expression of cleaved caspase-3, and downregulated Bcl-2/Bax ratio after OGD insult.
For vivo assay, the expressions of endogenous Ang II and AT1R gradually increased and peaked at 24 h after HIE.
Ang II increased NeuN-positive AT1R cell expression.
In addition, Ang II increased the area of cerebral infarction, promoted neuronal degeneration and apoptosis, aggravated neurological deficits on righting and geotaxis reflexes, and was accompanied by increased expressions of phosphorylated GSK-3β and mTOR.
The application of valsartan (Ang II inhibitor) or SB216763 (GSK-3β inhibitor) reversed these phenomena triggered by Ang II following HIE.
Conclusion.
Ang II increased neuronal apoptosis through the AT1R/GSK-3β/mTOR signaling pathway after experimental HIE both in vitro and in vivo, and Ang II may serve as a novel therapeutic target to ameliorate brain injury after HIE.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Si, Wei& Li, Banghui& Lenahan, Cameron& Li, Shirong& Gu, Ran& Qu, Hao…[et al.]. 2020. AT1RGSK-3βmTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1205806
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Si, Wei…[et al.]. AT1RGSK-3βmTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-14.
https://search.emarefa.net/detail/BIM-1205806
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Si, Wei& Li, Banghui& Lenahan, Cameron& Li, Shirong& Gu, Ran& Qu, Hao…[et al.]. AT1RGSK-3βmTOR Signaling Pathway Involved in Angiotensin II-Induced Neuronal Apoptosis after HIE Both In Vitro and In Vivo. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-14.
https://search.emarefa.net/detail/BIM-1205806
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1205806
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