Abstract
Saffron, an extract from Crocus sativus, has been largely used in traditional medicine for its antiapoptotic and anticarcinogenic properties. In this work, we investigate the effects of safranal, a component of saffron stigmas, in attenuating retinal degeneration in the P23H rat model of autosomal dominant retinitis pigmentosa. We demonstrate that administration of safranal to homozygous P23H line-3 rats preserves both photoreceptor morphology and number. Electroretinographic recordings showed higher a- and b-wave amplitudes under both photopic and scotopic conditions in safranal-treated versus non-treated animals. Furthermore, the capillary network in safranal-treated animals was preserved, unlike that found in untreated animals. Our findings indicate that dietary supplementation with safranal slows photoreceptor cell degeneration and ameliorates the loss of retinal function and vascular network disruption in P23H rats. This work also suggests that safranal could be potentially useful to retard retinal degeneration in patients with retinitis pigmentosa.
Highlights
Retinitis pigmentosa (RP) refers to a heterogeneous group of inherited neurodegenerative retinal disorders that cause progressive peripheral vision loss and poor night vision, which eventually leads to central vision impairment
Our study revealed that systemic treatment with safranal, a constituent of saffron (Crocus sativus), is capable of preserving retinal structure and function in homozygous P23H transgenic rats
It has been demonstrated that saffron extracts protect against ocular degenerative disorders caused by exposure to bright light [33] or age-related macular degeneration [34]
Summary
Retinitis pigmentosa (RP) refers to a heterogeneous group of inherited neurodegenerative retinal disorders that cause progressive peripheral vision loss and poor night vision, which eventually leads to central vision impairment. RP has been related to more than 100 different mutations of the rhodopsin-encoding gene (RHO), which altogether account for 30–40% of autosomal dominant cases. In the United States, this mutation alone accounts for about 12% of autosomal dominant RP cases [2]. The majority of RP-causing mutations in the RHO gene, including P23H, cause misfolding and retention of rhodopsin in the endoplasmic reticulum of transfected cultured cells [3]. These studies suggest that the RP mechanism may involve a cellular stress response [4] resulting in programmed photoreceptor cell death or apoptosis, a final common pathway for different retinal diseases [5]
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