دورية أكاديمية
Gardenamide A Protects RGC-5 Cells from H2O2-Induced Oxidative Stress Insults by Activating PI3K/Akt/eNOS Signaling Pathway
العنوان: | Gardenamide A Protects RGC-5 Cells from H2O2-Induced Oxidative Stress Insults by Activating PI3K/Akt/eNOS Signaling Pathway |
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المؤلفون: | Rikang Wang, Lizhi Peng, Jiaqiang Zhao, Laitao Zhang, Cuiping Guo, Wenhua Zheng, Heru Chen |
المصدر: | International Journal of Molecular Sciences, Vol 16, Iss 9, Pp 22350-22367 (2015) |
بيانات النشر: | MDPI AG, 2015. |
سنة النشر: | 2015 |
المجموعة: | LCC:Biology (General) LCC:Chemistry |
مصطلحات موضوعية: | gardenamide A, oxidative stress, cell apoptosis, neuroprotection, neurotoxicity, Biology (General), QH301-705.5, Chemistry, QD1-999 |
الوصف: | Gardenamide A (GA) protects the rat retinal ganglion (RGC-5) cells against cell apoptosis induced by H2O2. The protective effect of GA was completely abrogated by the specific phosphoinositide 3-kinase (PI3K) inhibitor LY294002, and the specific protein kinase B (Akt) inhibitor Akt VIII respectively, indicating that the protective mechanism of GA is mediated by the PI3K/Akt signaling pathway. The specific extracellular signal-regulated kinase (ERK1/2) inhibitor PD98059 could not block the neuroprotection of GA. GA attenuated the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) induced by H2O2. Western blotting showed that GA promoted the phosphorylation of ERK1/2, Akt and endothelial nitric oxide synthase (eNOS), respectively, and effectively reversed the H2O2-inhibited phosphorylation of these three proteins. LY294002 completely inhibited the GA-activated phosphorylation of Akt, while only partially inhibiting eNOS. This evidence implies that eNOS may be activated directly by GA. PD98059 attenuated only partially the GA-induced phosphorylation of ERK1/2 with/without the presence of H2O2, indicating that GA may activate ERK1/2 directly. All these results put together confirm that GA protects RGC-5 cells from H2O2 insults via the activation of PI3K/Akt/eNOS signaling pathway. Whether the ERK1/2 signaling pathway is involved requires further investigations. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1422-0067 |
Relation: | http://www.mdpi.com/1422-0067/16/9/22350; https://doaj.org/toc/1422-0067 |
DOI: | 10.3390/ijms160922350 |
URL الوصول: | https://doaj.org/article/48c493bc28824734a2a0d44b770a34d3 |
رقم الأكسشن: | edsdoj.48c493bc28824734a2a0d44b770a34d3 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 14220067 |
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DOI: | 10.3390/ijms160922350 |