Carnosic acid slows photoreceptor degeneration in the Pde6brd10 mouse model of retinitis pigmentosa

被引：57
作者：
Kang, Kai [1 ]
Tarchick, Matthew J. [1 ,2 ]
Yu, Xiaoshan [1 ]
Beight, Craig [1 ,2 ]
Bu, Ping [3 ]
Yu, Minzhong [1 ,4 ]
机构：
[1] Cleveland Clin Fdn, Cole Eye Inst, Dept Ophthalm Res, 9500 Euclid Ave, Cleveland, OH 44195 USA
[2] Louis Stokes Cleveland Vet Affairs Med Ctr, Cleveland, OH USA
[3] Loyola Univ Chicago, Dept Ophthalmol, Maywood, IL USA
[4] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Dept Ophthalmol, Cleveland, OH USA
来源：
SCIENTIFIC REPORTS | 2016年 / 6卷
关键词：
ENDOPLASMIC-RETICULUM STRESS; CHRONIC INFLAMMATORY REACTION; PROGRAMMED CELL-DEATH; RETINAL DEGENERATION; OXIDATIVE STRESS; BETA-SUBUNIT; ELECTROPHILIC COMPOUND; ROD PHOSPHODIESTERASE; PROTEIN-KINASE; BRAIN-INJURY;
D O I：
10.1038/srep22632
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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.
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页数：10
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