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Genipin Derivatives Protect RGC-5 from Sodium Nitroprusside-Induced Nitrosative Stress

التفاصيل البيبلوغرافية
العنوان: Genipin Derivatives Protect RGC-5 from Sodium Nitroprusside-Induced Nitrosative Stress
المؤلفون: Rikang Wang, Jiaqiang Zhao, Lei Zhang, Lizhi Peng, Xinyi Zhang, Wenhua Zheng, Heru Chen
المصدر: International Journal of Molecular Sciences, Vol 17, Iss 1, p 117 (2016)
بيانات النشر: MDPI AG, 2016.
سنة النشر: 2016
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: NO neurotoxicity, neuroprotection, neurodegeneration, apoptosis, genipin, nitric oxide synthase, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: CHR20 and CHR21 are a pair of stable diastereoisomers derived from genipin. These stereoisomers are activators of neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS). In the rat retinal ganglion (RGC-5) cell model these compounds are non-toxic. Treatment of RGC-5 with 750 μM of sodium nitroprusside (SNP) produces nitrosative stress. Both genipin derivatives, however, protect these cells against SNP-induced apoptic cell death, although CHR21 is significantly more potent than CHR20 in this regard. With Western blotting we showed that the observed neuroprotection is primarily due to the activation of protein kinase B (Akt)/eNOS and extracellular signal-regulated kinase (ERK1/2) signaling pathways. Therefore, LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor) or PD98059 (a MAPK-activating enzyme inhibitor) abrogated the protective effects of CHR20 and CHR21. Altogether, our results show that in our experimental setup neuroprotection by the diasteromeric pair is mediated through the PI3K/Akt/eNOS and ERK1/2 signaling pathways. Further studies are needed to establish the potential of these compounds to prevent ntric oxide (NO)-induced toxicity commonly seen in many neurodegenerative diseases.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: http://www.mdpi.com/1422-0067/17/1/117; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms17010117
URL الوصول: https://doaj.org/article/b60ad8fbb264415abecd9ea543c469ba
رقم الأكسشن: edsdoj.b60ad8fbb264415abecd9ea543c469ba
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms17010117