An in vivo study of cigarette smoke induced meibomian gland deterioration in a murine model.

Abstract

Objective: To investigate the effects of cigarette smoke (CS) exposure on the histopathological structure of the meibomian gland in a murine model, including the presence of inflammatory mediators and sebocyte apoptosis, and to provide a new experimental basis and theoretical support to further explore the relationship between CS and dry eye.

Methods: Forty-eight female C57BL/6 mice aged 6-8 weeks were randomly divided into a normal control group (12 weeks, 24 weeks) and a CS exposure group (12 weeks, 24 weeks). The normal control group received no treatment while the CS exposure group were exposed to CS 2 cigarettes/hour, 3 h/day and 6 days/week for either 12 or 24 weeks. Corneal changes were monitored regularly. Following CS exposure, meibomian gland tissues of mice were processed for H&E staining, CD45 immunohistochemical staining, and immunofluorescence staining for IL-6 and Ki67. The expression of IL-6, Ki67, P63, MMP-3 in meibomian glands were evaluated by RT-PCR. Sebocyte apoptosis was assessed through TUNEL staining.

Results: Compared with the normal control group, H&E staining in the CS12 group showed no significant change, while meibomian gland orifices were blocked in the CS24 group. TUNEL staining demonstrated a significant increase in cellular apoptosis in both smoke-exposed groups compared to the normal control group. IL-6 and MMP-3 were significantly up-regulated in meibomian gland tissues after 12 weeks of CS exposure and the expression of cell proliferation-related gene Ki67 and P63 decreased.

Conclusion: CS exposure induces meibomian gland inflammation, promotes sebocyte apoptosis, and inhibits sebocyte proliferation in mice.