Abstract
Coenzyme Q10 (CoQ10) is a mitochondrial-targeted antioxidant with known neuroprotective activity. Its ocular effects when co-solubilised with α–tocopherol polyethylene glycol succinate (TPGS) were evaluated. In vitro studies confirmed that CoQ10 was significantly protective in different retinal ganglion cell (RGC) models. In vivo studies in Adult Dark Agouti (DA) rats with unilateral surgically-induced ocular hypertension (OHT) treated with either CoQ10/TPGS micelles or TPGS vehicle twice daily for three weeks were performed, following which retinal cell health was assessed in vivo using DARC (Detection of Apoptotic Retinal Cells) and post-mortem with Brn3a histological assessment on whole retinal mounts. CoQ10/TPGS showed a significant neuroprotective effect compared to control with DARC (p<0.05) and Brn3 (p<0.01). Topical CoQ10 appears an effective therapy preventing RGC apoptosis and loss in glaucoma-related models.
Highlights
Glaucoma is a progressive neurodegenerative eye disorder estimated to affect 60 million people worldwide (Cook and Foster, 2012; Tham et al, 2014)
Glaucoma involves the progressive loss of retinal ganglion cells (RGCs) and their axons, which results in visual field abnormalities and blindness if left untreated (GarciaValenzuela et al, 1995; Quigley et al, 1995)
Coenzyme Q10 (CoQ10)/tocopherol polyethylene glycol succinate (TPGS) but not TPGS treatment alone could protect rat retinal RGCs against intraocular pressure (IOP)-induced apoptosis as indicated by the preservation in RGC density (Fig. 6A & B) and nearest neighbour distance (Fig. 6C & D) in the CoQ10/TPGS treated groups versus TPGS only or untreated (OHT only) controls. This study uses both in vitro and in vivo mitochondrial-mediated neurotoxicity models to successfully demonstrate the neuroprotective activity of CoQ10/TPGS compared to TPGS alone
Summary
Glaucoma is a progressive neurodegenerative eye disorder estimated to affect 60 million people worldwide (Cook and Foster, 2012; Tham et al, 2014). Glaucoma involves the progressive loss of retinal ganglion cells (RGCs) and their axons, which results in visual field abnormalities and blindness if left untreated (GarciaValenzuela et al, 1995; Quigley et al, 1995). RGC loss in glaucoma is predominantly thought to occur via elevated apoptosis (a type of programmed cell death) (Quigley et al, 1995; Cordeiro et al, 2010) which is mainly mitochondrial dysfunction mediated (Lee et al, 2014a; Ju et al, 2008; Park et al, 2011). Mitochondria are a source and target of oxidative stress and are key in the development of neuroprotective strategies for RGC preservation in glaucoma (Chrysostomou et al, 2013)
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