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Int. J. Mol. Sci. 2016, 17(1), 117; doi:10.3390/ijms17010117

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

1
National Pharmaceutical Engineering Center for Solid Preparation in Chinese Herbal Medicine, Jiangxi University of Traditional Chinese Medicine, Nanchang 330006, China
2
Institute of Traditional Chinese Medicine and Natural Products, College of Pharmacy, Jinan University, Guangzhou 510632, China
3
Faculty of Health Sciences, University of Macao, Macao, China
4
Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Guangzhou 510632, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Katalin Prokai-Tatrai
Received: 20 October 2015 / Revised: 26 November 2015 / Accepted: 8 January 2016 / Published: 19 January 2016
(This article belongs to the Special Issue Neuroprotective Strategies 2015)
View Full-Text   |   Download PDF [3037 KB, uploaded 19 January 2016]   |  

Abstract

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. View Full-Text
Keywords: NO neurotoxicity; neuroprotection; neurodegeneration; apoptosis; genipin; nitric oxide synthase NO neurotoxicity; neuroprotection; neurodegeneration; apoptosis; genipin; nitric oxide synthase
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Wang, R.; Zhao, J.; Zhang, L.; Peng, L.; Zhang, X.; Zheng, W.; Chen, H. Genipin Derivatives Protect RGC-5 from Sodium Nitroprusside-Induced Nitrosative Stress. Int. J. Mol. Sci. 2016, 17, 117.

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