Targeting Nrf2 signaling in dry eye

Dry eye,the most common ocular surface disease,can cause ocular surface tissue damage and discomfort symptoms and seriously affect people’s quality of life.The etiology of dry eye is diverse,and its pathogenesis is complex.The oxidative stress reaction is considered to be among the important factors in the pathogenesis of dry eye.Therefore,activating the antioxidant system has a potential therapeutic effect on dry eye.Nuclear factor erythroid 2-related factor 2(Nrf2)signaling pathway is considered the most important antioxidant pathway in the body.The activation of the Nrf2 signaling pathway and its interaction with other pathways are important mechanisms to prevent the occurrence and development of dry eye.This review describes the structure and function of Nrf2,summarizes the changes in the oxidative stress response in dry eye,focuses on the potential mechanism of the Nrf2 signaling pathway in the treatment of dry eye,and,finally,summarizes the drugs that activate the Nrf2 signaling pathway in the treatment of dry eye.

Alkali burn injury model of meibomian gland dysfunction in mice

AIM:To establish a stable,short-time,low-cost and reliable murine model of meibomian gland dysfunction(MGD).METHODS:A filter paper sheet soaked in 1.0 mol/L sodium hydroxide(NaOH)solution was used to touch the eyelid margin of C57BL/6J mice for 10s to establish the model.The other eye was left untreated as a control group.Eyelid margin morphological changes and the meibomian glands(MGs)were observed by slit lamp microscopy on days 5 and 10 post-burn.Hematoxylin-eosin(HE)staining and Oil red O staining were adopted in detecting the changes in MGs morphology and lipid deposition.Real-time polymerase chain reaction,Western blot,immunofluorescence staining and immunohistochemical staining were used to detect interleukin(IL)-6,IL-1β,IL-18,tumor necroses factor(TNF)-α,interferon(IFN)-γ,nicotinamide adenine dinucleotide phosphate(NADPH)oxidase 4(NOX4),3-nitroturosine(3-NT),4-hydroxynonenal(4-HNE)and cytokeratin 10(K10)expression changes in MGs.RESULTS:MGs showed plugging of orifice,glandular deficiency,abnormal acinar morphology,ductal dilatation,and lipid deposition after alkali burn.The expressions of IL-6,IL-18,IL-1β,IFN-γ,and TNF-αindicators of inflammation and oxidative stress in MGs tissues were significantly increased.Abnormal keratinization increased in the MG duct.CONCLUSION:A murine model of MGD is established by alkali burn of the eyelid margin that matches the clinical presentation of MGD providing a stable,short-time,lowcost,and reliable MGD model.The new method suggests efficient avenues for future research.