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Calcitriol, the Active Metabolite of Vitamin D 3 , Inhibits Dry Eye Related Corneal Inflammation In Vivo and In Vitro.
Ocular Immunology and Inflammation 2017 October 18
PURPOSE: To examine the influence of topical administration of calcitriol on dry eye (DE) related corneal inflammation.
METHODS: Benzalkonium chloride (BAC, 0.2%) was applied to induce DE. Then rats were treated topically with calcitriol (10-6 μM). Tear break-up time (TBUT), fluorescein staining score, inflammatory index, and tear volume were measured. Corneal epithelium damage and corneal inflammation were examined by H&E staining or RT-qPCR. In vitro, human corneal epithelial cells (iHCEC) were cultured in hyperosmotic medium (450 mOsM) with various concentrations of calcitriol. Levels of pro-inflammatory mediators were measured by RT-qPCR or ELISA. NF-κB activation was examined by Western blotting and immunofluorescence staining.
RESULTS: Calcitriol significantly ameliorated DE symptoms, attenuating corneal inflammation. In vitro studies showed that calcitriol significantly decreased the expression of pro-inflammatory mediators in iHCECs under hyperosmotic stress, probably through inhibiting NF-κB activation.
CONCLUSION: The results suggest that calcitriol might be a potential therapeutic agent for DE.
METHODS: Benzalkonium chloride (BAC, 0.2%) was applied to induce DE. Then rats were treated topically with calcitriol (10-6 μM). Tear break-up time (TBUT), fluorescein staining score, inflammatory index, and tear volume were measured. Corneal epithelium damage and corneal inflammation were examined by H&E staining or RT-qPCR. In vitro, human corneal epithelial cells (iHCEC) were cultured in hyperosmotic medium (450 mOsM) with various concentrations of calcitriol. Levels of pro-inflammatory mediators were measured by RT-qPCR or ELISA. NF-κB activation was examined by Western blotting and immunofluorescence staining.
RESULTS: Calcitriol significantly ameliorated DE symptoms, attenuating corneal inflammation. In vitro studies showed that calcitriol significantly decreased the expression of pro-inflammatory mediators in iHCECs under hyperosmotic stress, probably through inhibiting NF-κB activation.
CONCLUSION: The results suggest that calcitriol might be a potential therapeutic agent for DE.
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