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Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling
المؤلفون المشاركون
Cai, Hui
Li, Xiaojun
Yao, Li
Liang, Qianlei
Qu, Hangyin
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
2018-06-26
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Objectives.
Propofol is a popular anesthetic drug that is neuroprotective.
However, the mechanisms of propofol for hippocampal neuroprotection remain elusive.
This study is aimed at investigating the neuroprotective effect and mechanism of propofol in hippocampal neurons exposed to ischemia-reperfusion (I/R) injury.
Methods.
Hypoxia-reoxygenated (H/R) HT-22 cells were used to mimic I/R injury of the hippocampus in vitro.
An MTT assay was used to determine cell viability.
Cell apoptosis was detected by a TUNEL assay and a flow cytometry cell apoptosis assay.
Expression levels of proteins were measured by Western blotting.
Intracellular calcium was assessed by Fura-2/AM staining.
Flow cytometry was used to determine the mitochondrial membrane potential (MMP).
Coimmunoprecipitation was used to evaluate the stability of the FKBP-RyR complex.
Calcineurin enzymatic activity was measured with a colorimetric method.
YAP nuclear translocation was tested by immunofluorescence staining.
Results.
H/R induced HT-22 cell viability depression, and apoptosis was reversed by propofol treatment.
Propofol could alleviate H/R-induced intracellular calcium accumulation and MMP loss by inhibiting calcineurin activity and FKBP12.6-RyR disassociation in a concentration-dependent manner.
In addition, YAP expression was crucial for propofol to protect HT-22 cell apoptosis from H/R injury.
Propofol could activate YAP through dephosphorylation.
Activated YAP stimulated the transcription of the Bcl2 gene, which promotes cellular survival.
Our data also demonstrated that propofol activated YAP through the RhoA-Lats1 pathway without large G proteins or MST involvement.
In addition, we showed that there was no interaction between calcineurin signaling and YAP activation in HT-22 cells.
Conclusions.
Propofol protected hippocampal neurons from I/R injury through two independent signaling pathways, including the calcineurin/FKBP12.6-RyR/calcium overload pathway and the RhoA/Lats1/YAP/Bcl-2 pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Li, Xiaojun& Yao, Li& Liang, Qianlei& Qu, Hangyin& Cai, Hui. 2018. Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1210904
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Li, Xiaojun…[et al.]. Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-12.
https://search.emarefa.net/detail/BIM-1210904
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Li, Xiaojun& Yao, Li& Liang, Qianlei& Qu, Hangyin& Cai, Hui. Propofol Protects Hippocampal Neurons from Hypoxia-Reoxygenation Injury by Decreasing Calcineurin-Induced Calcium Overload and Activating YAP Signaling. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-12.
https://search.emarefa.net/detail/BIM-1210904
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1210904
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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