Kang Kai, Tarchick Matthew J, Yu Xiaoshan, Beight Craig, Bu Ping, Yu Minzhong
Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland OH, USA.
Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, OH, USA.
Sci Rep. 2016 Mar 10;6:22632. doi: 10.1038/srep22632.
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.
与各种遗传性视网膜色素变性(RP)相关的光感受器细胞死亡目前无法治疗,并会导致部分或完全视力丧失。肌醇六磷酸(CA)可上调内源性抗氧化酶,并且在影响大脑的神经退行性模型研究中已证明具有神经保护作用。在本研究中,我们检测了CA对RP的Pde6b(rd10)小鼠模型中光感受器死亡的潜在影响。我们的数据表明,CA可对光感受器起到形态和功能上的保护作用。CA似乎通过抑制氧化应激和内质网应激来发挥其神经保护作用。