Abstract
Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs). Strategies that delay or halt RGC loss have been recognized as potentially beneficial for rescuing vision in glaucoma patients. Quercetin (Qcn) is a natural and important dietary flavonoid compound, widely distributed in fruits and vegetables. Mounting evidence suggests that Qcn has numerous neuroprotective effects. However, whether Qcn exerts neuroprotective effects on RGC in glaucoma is poorly understood. In this study, we investigated the protective effect of Qcn against RGC damage in a rat chronic ocular hypertension (COHT) model in vivo and hypoxia-induced primary cultured RGC damage in vitro, and we further explored the underlying neuroprotective mechanisms. We found that Qcn not only improved RGC survival and function from a very early stage of COHT in vivo, it promoted the survival of hypoxia-treated primary cultured RGCs in vitro via ameliorating mitochondrial function and preventing mitochondria-mediated apoptosis. Our findings suggest that Qcn has direct protective effects on RGCs that are independent of lowering the intraocular pressure (IOP). Qcn may be a promising therapeutic agent for improving RGC survival and function in glaucomatous neurodegeneration.
Highlights
Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs), and it is a major cause of irreversible visual impairment worldwide, as damaged RGCs are incapable of repair or regeneration (Calkins, 2012)
These results demonstrated that chronic ocular hypertension (COHT) is effectively induced by the anterior chamber injection of microbeads in rats, which is similar to human ocular hypertension and chronic glaucoma
We investigated the protective effect of Qcn against RGC damage using a rat COHT model in vivo and explored the underlying molecular mechanism by hypoxia-induced primary cultured RGC damage in vitro
Summary
Glaucoma is a progressive neuropathy characterized by the loss of retinal ganglion cells (RGCs), and it is a major cause of irreversible visual impairment worldwide, as damaged RGCs are incapable of repair or regeneration (Calkins, 2012). Strategies that delay or halt RGC loss have been recognized as potentially helpful for rescuing vision in glaucoma. Quercetin Protect RGC in Glaucoma agents have been identified, such as N-methyl-D-aspartate (NMDA) receptor antagonists (memantine and brimonidine), glutamate release inhibitors (bis(7)-tacrine; Fang et al, 2010), calcium channel blockers (cilnidipine and lomerizine; Fitzgerald et al, 2009), neurotrophins (brain-derived neurotrophic factor and neurotrophic factor; Pease et al, 2009), antioxidants (astaxanthin and flavonoids; Yamagishi and Aihara, 2014), and others, which can be used alone or in combination with intraocular pressure (IOP)-lowering therapy. It is imperative to identify more efficacious neuroprotective agents with potential clinical value for preventing or slowing down RGC loss as well as for preserving RGC function for multiple or, ideally, all mechanisms of glaucoma (Levin and Danesh-Meyer, 2010)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
