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Ectoine, a novel natural osmoprotectant, protects bacteria living in extreme environments. This study aimed to explore the therapeutic effect of ectoine for dry eye disease. An experimental dry eye model was created in C57BL/6 mice exposed to desiccating stress (DS) with untreated mice as controls (UT). DS mice were dosed topically with 0.5–2.0% of ectoine or a vehicle control. Corneal epithelial defects were detected via corneal smoothness and Oregon Green dextran (OGD) fluorescent staining. Pro-inflammatory cytokines and chemokines were evaluated using RT-qPCR and immunofluorescent staining. Compared with UT mice, corneal epithelial defects were observed as corneal smoothness irregularities and strong punctate OGD fluorescent staining in DS mice with vehicle. Ectoine treatment protected DS mice from corneal damage in a concentration-dependent manner, and ectoine at 1.0 and 2.0% significantly restored the corneal smoothness and reduced OGD staining to near normal levels. Expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokines CCL3 and CXCL11 was significantly elevated in the corneas and conjunctivas of DS mice, whereas 1.0 and 2.0% ectoine suppressed these inflammatory mediators to near normal levels. Our findings demonstrate that ectoine can significantly reduce the hallmark pathologies associated with dry eye and may be a promising candidate for treating human disease.

AIM: To assess the retinal vasculature alterations in indirect traumatic optic neuropathy (ITON) patients following craniofacial trauma by optic coherence tomography angiography (OCTA). METHODS: Patients diagnosed of monocular ITON were recruited from August 2016 to May 2020. OCTA was performed using the AngioVue OCT-A system for two cube scans centered at the optic nerve head and fovea. OCTA data included thicknesses of peripapillary retinal nerve fiber layer (RNFL) and macular ganglion cell complex (GCC), as well as proportion of capillary perfusion and data were analyzed for correlation with post-injury timepoints: within 7, 8-30, 31-90, and 91-365d. RESULTS: A total of 73 ITON patients were studied. Significant thinning of RNFL and GCC layers and attenuation of microvascular perfusion were observed in ITON eyes as compared to contralateral unaffected eyes (for most of the analyzed sectors and quadrants, P

AIM:To seek a small interfering RNA(siRNA)sequence targeting rat inhibitor of nuclear factor kappa B α(IκBα)that can specifically and effectively suppress IκBα mRNA expression of rat ciliary muscles in vivo.METHODS:Three IκBα specific double stranded siRNAs were designed and synthesized. They were transfected into rat A7r5 cells which express IκBα gene. Flow cytometry was used to assess transfected efficiency. The mRNA and protein levels of IκBα were examined by Real Time quantitative polymerase chain reaction(Real Time-PCR)and western blot to screen a candidate valid sequence with the highest inhibitory rate. The Cy3 labeled non-specific control siRNA or the candidate valid siRNA was then injected into rat anterior chamber. Distribution of Cy3-siRNA in rat ciliary muscles was viewed by fluorescence microscopy, and the inhibitory effect in vivo of the valid siRNA was identified via Real Time-PCR and immunofluorescence.RESULTS: The suppression effect of the siRNA targeting the CTACGATGACTGTGTGTTT of IκBα gene was most obvious by vitro screening. By anterior chamber injection, this valid siRNA could reach rat ciliary muscles and effectively suppress IκBα gene expression with the highest inhibitory rate of 59.0% on mRNA level at 24h after RNAi, and 52.3% on protein level at 72h after RNAi(PCONCLUSION: It proves that the siRNA targeting the CTACGATGACTGTGTGTTT of IκBα gene is the valid sequence to suppress rat IκBα expression of ciliary muscles by RNAi in vivo.