Carnosic acid slows photoreceptor degeneration in the Pde6b(rd10) mouse model of retinitis pigmentosa

The photoreceptor cell death associated with the various genetic forms of retinitis pigmentosa (RP) is currently untreatable and leads to partial or complete vision loss. Carnosic acid (CA) upregulates endogenous antioxidant enzymes and has proven neuroprotective in studies of neurodegenerative mode...

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Veröffentlicht in:	Scientific reports 2016-03, Vol.6, p.22632-22632
Hauptverfasser:	Kang, Kai, Tarchick, Matthew J, Yu, Xiaoshan, Beight, Craig, Bu, Ping, Yu, Minzhong
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antioxidants - pharmacology Antioxidants - therapeutic use Cyclic Nucleotide Phosphodiesterases, Type 6 - genetics Diterpenes, Abietane - pharmacology Diterpenes, Abietane - therapeutic use Endoplasmic Reticulum Stress Mice Mice, Inbred C57BL Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Photoreceptor Cells - drug effects Photoreceptor Cells - metabolism Photoreceptor Cells - pathology Retinitis Pigmentosa - drug therapy Retinitis Pigmentosa - genetics
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Zusammenfassung:	The photoreceptor cell death associated with the various genetic forms of retinitis pigmentosa (RP) is currently untreatable and leads to partial or complete vision loss. Carnosic acid (CA) upregulates endogenous antioxidant enzymes and has proven neuroprotective in studies of neurodegenerative models affecting the brain. In this study, we examined the potential effect of CA on photoreceptor death in the Pde6b(rd10) mouse model of RP. Our data shows that CA provided morphological and functional preservation of photoreceptors. CA appears to exert its neuroprotective effects through inhibition of oxidative stress and endoplasmic reticulum stress.
ISSN:	2045-2322
DOI:	10.1038/srep22632