Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κBHif-1α Signaling
المؤلفون المشاركون
Peng, Xiaowei
Li, Chenglong
Yu, Wei
Liu, Shuai
Cong, Yushuang
Fan, Guibo
Qi, Sihua
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-04-28
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Hypoxia-induced neuroinflammation typically causes neurological damage and can occur during stroke, neonatal hypoxic-ischemic encephalopathy, and other diseases.
Propofol is widely used as an intravenous anesthetic.
Studies have shown that propofol has antineuroinflammatory effect.
However, the underlying mechanism remains to be fully elucidated.
Thus, we aimed to investigate the beneficial effects of propofol against hypoxia-induced neuroinflammation and elucidated its potential cellular and biochemical mechanisms of action.
In this study, we chose cobalt chloride (CoCl2) to establish a hypoxic model.
We found that propofol decreased hypoxia-induced proinflammatory cytokines (TNFα, IL-1β, and IL-6) in BV2 microglia, significantly suppressed the excessive production of reactive oxygen species, and increased the total antioxidant capacity and superoxide dismutase activity.
Furthermore, propofol attenuated the hypoxia-induced decrease in mitochondrial membrane potential andy 2 strongly inhibited protein expression of nuclear factor-kappa B (NF-κB) subunit p65 and hypoxia inducible factor-1α (Hif-1α) in hypoxic BV2 cells.
To investigate the role of NF-κB p65, specific small interfering RNA (siRNA) against NF-κB p65 were transfected into BV2 cells, followed by exposure to hypoxia for 24 h.
Hypoxia-induced Hif-1α production was downregulated after NF-κB p65 silencing.
Further, propofol suppressed Hif-1α expression by inhibiting the upregulation of NF-κB p65 after exposure to hypoxia in BV2 microglia.
In summary, propofol attenuates hypoxia-induced neuroinflammation, at least in part by inhibiting oxidative stress and NF-κB/Hif-1α signaling.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Peng, Xiaowei& Li, Chenglong& Yu, Wei& Liu, Shuai& Cong, Yushuang& Fan, Guibo…[et al.]. 2020. Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κBHif-1α Signaling. BioMed Research International،Vol. 2020, no. 2020, pp.1-11.
https://search.emarefa.net/detail/BIM-1137899
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Peng, Xiaowei…[et al.]. Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κBHif-1α Signaling. BioMed Research International No. 2020 (2020), pp.1-11.
https://search.emarefa.net/detail/BIM-1137899
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Peng, Xiaowei& Li, Chenglong& Yu, Wei& Liu, Shuai& Cong, Yushuang& Fan, Guibo…[et al.]. Propofol Attenuates Hypoxia-Induced Inflammation in BV2 Microglia by Inhibiting Oxidative Stress and NF-κBHif-1α Signaling. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-11.
https://search.emarefa.net/detail/BIM-1137899
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1137899
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