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-α indicators 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, low-cost, and reliable MGD model. The new method suggests efficient avenues for future research.