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Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C
المؤلفون المشاركون
Jia, Ji
Peng, Jie
Li, Zhaoju
Wu, Youping
Wu, Qunlin
Wu, Mingchun
Tu, Weifeng
المصدر
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-01-13
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Background.
Reducing β amyloid- (Aβ-) induced microglial activation is considered to be effective in treating Alzheimer’s disease (AD).
Nicotine attenuates Aβ-induced microglial activation; the mechanism, however, is still elusive.
Microglia could be activated into classic activated state (M1 state) or alternative activated state (M2 state); the former is cytotoxic and the latter is neurotrophic.
In this investigation, we hypothesized that nicotine attenuates Aβ-induced microglial activation by shifting microglial M1 to M2 state, and cannabinoid CB2 receptor and protein kinase C mediate the process.
Methods.
We used Aβ1–42 to activate N9 microglial cells and observed nicotine-induced effects on microglial M1 and M2 biomarkers by using western blot, immunocytochemistry, and enzyme-linked immunosorbent assay (ELISA).
Results.
We found that nicotine reduced the levels of M1 state markers, including inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor α (TNF-α) and interleukin- (IL-) 6 releases; meanwhile, it increased the levels of M2 state markers, including arginase-1 (Arg-1) expression and brain-derived neurotrophic factor (BDNF) release, in the Aβ-stimulated microglia.
Coadministration of cannabinoid CB2 receptor antagonist or protein kinase C (PKC) inhibitor partially abolished the nicotine-induced effects.
Conclusion.
These findings indicated that cannabinoid CB2 receptor mediates nicotine-induced anti-inflammation in microglia exposed to Aβ via PKC.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Jia, Ji& Peng, Jie& Li, Zhaoju& Wu, Youping& Wu, Qunlin& Tu, Weifeng…[et al.]. 2016. Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C. Mediators of Inflammation،Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1111076
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Jia, Ji…[et al.]. Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C. Mediators of Inflammation No. 2016 (2016), pp.1-10.
https://search.emarefa.net/detail/BIM-1111076
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Jia, Ji& Peng, Jie& Li, Zhaoju& Wu, Youping& Wu, Qunlin& Tu, Weifeng…[et al.]. Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C. Mediators of Inflammation. 2016. Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1111076
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1111076
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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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
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