Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0314719 (dry eye)
 2,625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Decreases in tear volume, unstable tear films and excessive tear evaporation are known to cause desiccation and hyperosmolar stress. These, in turn, induce oxidative stress that is thought to cause dry eye, which is also considered to be age-related disease. We hypothesized that oxidative stress induces up-regulation of age-related markers, and that the antioxidant astaxanthin prepared as a liposomal formulation may be a candidate for the treatment of dry eye. Herein, we examined age-related markers in an in vitro dry eye model, and evaluated the efficacy of high-affinity liposomes containing astaxanthin. The in vitro dry eye model showed desiccation time-dependent increases in reactive oxygen species. We confirmed the up-regulation of p53, p21 and p16 as a function of desiccation time. Pretreatment with both neutral and slightly-positively-charged astaxanthin liposomal formulations showed significant suppression of up-regulation of all markers, with the positively-charged liposomes exhibiting the greatest efficacy. Furthermore, positively-charged liposomes labeled with fluorescent dyes demonstrated much higher affinity to normal human corneal epithelial cells (HCECs) than neutral liposomes. Taken together, we confirmed the up-regulation of age-related markers, especially p16, in an in vitro dry eye model, and demonstrated the potential of high-affinity liposomal astaxanthin for the treatment of dry eye.
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PMID:Efficacy of high-affinity liposomal astaxanthin on up-regulation of age-related markers induced by oxidative stress in human corneal epithelial cells. 3070 9

Oxidative stress induced by decreases in tear volume and excessive tear evaporation is a key factor in dry eye disease (DED). Previously, we reported that desiccation stress induces reactive oxygen species generation and up-regulated expression of age-related markers such as p53, p21 and p16. We also showed that the antioxidant astaxanthin prepared as a liposomal formulation could suppress these phenomena in the in vitro DED model. In this study, we evaluated the protective effect of liposomes encapsulating astaxanthin against superficial punctate keratopathy (SPK) in the in vivo rat DED model. This model of DED was characterized by decreased tear volume and increased fluorescein score as an indicator of SPK as well as upregulated expression of age-related markers. Repeat-dose of liposomal astaxanthin prevented increases in the fluorescein score and up-regulation of age-related markers. Liposomes bearing a slight positive surface charge had superior effects and higher affinity compared to neutral liposomes. Furthermore, fluorescence intensities in rat corneal epithelium after administration of high-affinity liposomes labeled with fluorescent dye were higher than those for neutral liposomes. In conclusion, we developed the high-affinity liposomal formulation that can prevent DED and promote antioxidative effects of astaxanthin.
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PMID:Protective effect of high-affinity liposomes encapsulating astaxanthin against corneal disorder in the in vivo rat dry eye disease model. 3252 49