Attenuation of β-Amyloid-Induced Oxidative Cell Death by Sulforaphane via Activation of NF-E2-Related Factor 2
المؤلفون المشاركون
Lee, Chan
Jang, Jung-Hee
Lee, Seong-Ryong
Park, Gyu Hwan
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2013، العدد 2013 (31 ديسمبر/كانون الأول 2013)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2013-06-20
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
العلوم الطبيعية والحياتية (متداخلة التخصصات)
الأحياء
الملخص EN
β-amyloid peptide (Aβ), a major component of senile plaques, plays important roles in neuropathology of Alzheimer's disease (AD).
An array of in vitro and in vivo data indicates that Aβ-induced neuronal death is mediated by oxidative stress.
In this study, we aimed to investigate effects of sulforaphane (SUL), an isothiocyanate in cruciferous vegetables, on Aβ-induced oxidative cell death in SH-SY5Y cells.
Cells treated with Aβ25–35 exhibited decreased cell viability and underwent apoptosis as determined by MTT assay and TUNEL, respectively.
Aβ25–35-induced cytotoxicity and apoptotic characteristics such as activation of c-JNK, dissipation of mitochondrial membrane potential, altered expression of Bcl-2 family proteins, and DNA fragmentation were effectively attenuated by SUL pretreatment.
The antiapoptotic activity of SUL seemed to be mediated by inhibition of intracellular accumulation of reactive oxygen species and oxidative damages.
SUL exerted antioxidant potential by upregulating expression of antioxidant enzymes including γ-glutamylcysteine ligase, NAD(P)H:quinone oxidoreductase-1, and heme oxygenase-1 via activation of NF-E2-related factor 2(Nrf2).
The protective effect of SUL against Aβ25–35-induced apoptotic cell death was abolished by siRNA of Nrf2.
Taken together, the results suggest that pharmacologic activation of Nrf2 signaling pathway by SUL might be a practical prevention and/or protective treatment for the management of AD.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Lee, Chan& Park, Gyu Hwan& Lee, Seong-Ryong& Jang, Jung-Hee. 2013. Attenuation of β-Amyloid-Induced Oxidative Cell Death by Sulforaphane via Activation of NF-E2-Related Factor 2. Oxidative Medicine and Cellular Longevity،Vol. 2013, no. 2013, pp.1-12.
https://search.emarefa.net/detail/BIM-462640
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Lee, Chan…[et al.]. Attenuation of β-Amyloid-Induced Oxidative Cell Death by Sulforaphane via Activation of NF-E2-Related Factor 2. Oxidative Medicine and Cellular Longevity No. 2013 (2013), pp.1-12.
https://search.emarefa.net/detail/BIM-462640
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Lee, Chan& Park, Gyu Hwan& Lee, Seong-Ryong& Jang, Jung-Hee. Attenuation of β-Amyloid-Induced Oxidative Cell Death by Sulforaphane via Activation of NF-E2-Related Factor 2. Oxidative Medicine and Cellular Longevity. 2013. Vol. 2013, no. 2013, pp.1-12.
https://search.emarefa.net/detail/BIM-462640
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-462640
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