水液缺乏型干眼模型小鼠睑板腺的变化.

BACKGROUND: In recent years, increasing studies have focused on the abnormal proliferation and differentiation of acinous cells in the meibomian gland, suggesting that this process is closely related to the occurrence and development of dry eye. Structural and functional abnormalities such as blockage of the lumen of the meibomian gland and atrophy of the glands can cause or exacerbate dry eye. Therefore, the study of changes in the meibomian glands in dry eyes is important for understanding the pathogenesis of dry eyes in depth and finding new targets for the treatment and prevention of dry eyes. OBJECTIVE: To investigate the changes of the meibomian gland in a mouse model of aqueous deficient dry eyes. METHODS: Thirty-two female C57/B6 mice at 6-8 weeks were selected and randomly divided into experimental and control groups with 16 mice in each group. The mice in the experimental group were constructed by removing both the extra-orbital and intra-orbital lacrimal glands, while those in the control group were not treated. After 2 weeks of normal feeding, the corneal changes of both groups were observed under a slit lamp, and the tear secretion of both groups was measured. The meibomian glands of the two groups of mice were removed after decapitation. The changes in the gross morphology of the meibomian glands were observed and the meibomian glands were made into frozen sections. Hematoxylin-eosin staining was used to observe the structure of the meibomian glands, oil red staining was used to evaluate the function of the meibomian glands, and immunofluorescence staining and RT-qPCR were used to observe the expression of cytokeratin 14, Ki67 and abnormally differentiated small proline-rich protein 1B in the meibomian glands of mice. RESULTS AND CONCLUSION: Two weeks after modeling, lamellar defects were seen in the corneas of the experimental mice, and neovascularization of the limbal corneal was generated and invaded the central cornea. (2) Tear secretion volume was significantly reduced in the experimental group compared with the control group (P < 0.05). Microscopic findings showed that the ducts of the meibomian glands in the experimental group were interrupted and atrophied, and their arrangement was disorganized. Hematoxylin-eosin staining results showed a significant increase in lipid vacuoles in the meibomian glands of the experimental mice compared with the control group. Lipid deposition was seen in oil red staining in the experimental group. Immunofluorescence and RTqPCR results showed a significant increase in the expression of cytokeratin 14, Ki67 and small proline-rich protein 1B in the meibomian glands of mice in the experimental group compared with the control group (P < 0.05). To conclude, aqueous deficient dry eye can lead to compensatory hypertrophy, increased proliferation, and abnormal lipid metabolism in the meibomian gland, as well as abnormal differentiation of the meibomian gland. [ABSTRACT FROM AUTHOR]