AP39, a Mitochondria-Targeted Hydrogen Sulfide Donor, Supports Cellular Bioenergetics and Protects against Alzheimer’s Disease by Preserving Mitochondrial Function in APPPS1 Mice and Neurons
المؤلفون المشاركون
Yan, Ning
Zhao, Feng-li
Fang, Fang
Qiao, Pei-feng
Gao, Dan
Yan, Yong
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-19، 19ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-01-31
دولة النشر
مصر
عدد الصفحات
19
التخصصات الرئيسية
الملخص EN
Increasing evidence suggests that mitochondrial functions are altered in AD and play an important role in AD pathogenesis.
It has been established that H2S homeostasis is balanced in AD.
The emerging mitochondrial roles of H2S include antioxidation, antiapoptosis, and the modulation of cellular bioenergetics.
Here, using primary neurons from the well-characterized APP/PS1 transgenic mouse model, we studied the effects of AP39 (a newly synthesized mitochondrially targeted H2S donor) on mitochondrial function.
AP39 increased intracellular H2S levels, mainly in mitochondrial regions.
AP39 exerted dose-dependent effects on mitochondrial activity in APP/PS1 neurons, including increased cellular bioenergy metabolism and cell viability at low concentrations (25–100 nM) and decreased energy production and cell viability at a high concentration (250 nM).
Furthermore, AP39 (100 nM) increased ATP levels, protected mitochondrial DNA, and decreased ROS generation.
AP39 regulated mitochondrial dynamics, shifting from fission toward fusion.
After 6 weeks, AP39 administration to APP/PS1 mice significantly ameliorated their spatial memory deficits in the Morris water maze and NORT and reduced Aβ deposition in their brains.
Additionally, AP39 inhibited brain atrophy in APP/PS1 mice.
Based on these results, AP39 was proposed as a promising drug candidate for AD treatment, and its anti-AD mechanism may involve protection against mitochondrial damage.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Zhao, Feng-li& Fang, Fang& Qiao, Pei-feng& Yan, Ning& Gao, Dan& Yan, Yong. 2016. AP39, a Mitochondria-Targeted Hydrogen Sulfide Donor, Supports Cellular Bioenergetics and Protects against Alzheimer’s Disease by Preserving Mitochondrial Function in APPPS1 Mice and Neurons. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-19.
https://search.emarefa.net/detail/BIM-1114343
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Zhao, Feng-li…[et al.]. AP39, a Mitochondria-Targeted Hydrogen Sulfide Donor, Supports Cellular Bioenergetics and Protects against Alzheimer’s Disease by Preserving Mitochondrial Function in APPPS1 Mice and Neurons. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-19.
https://search.emarefa.net/detail/BIM-1114343
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Zhao, Feng-li& Fang, Fang& Qiao, Pei-feng& Yan, Ning& Gao, Dan& Yan, Yong. AP39, a Mitochondria-Targeted Hydrogen Sulfide Donor, Supports Cellular Bioenergetics and Protects against Alzheimer’s Disease by Preserving Mitochondrial Function in APPPS1 Mice and Neurons. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-19.
https://search.emarefa.net/detail/BIM-1114343
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1114343
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