睑板腺功能障碍（MGD）发病率逐年增加，其与年龄有显著相关性，这与中老年人睑板腺萎缩直接相关。现有临床治疗手段难以针对睑板腺萎缩进行有效治疗。我们研究发现小鼠睑板腺经过急性冷冻损伤后，其腺泡区域呈先减少后增加的趋势，最终恢复正常水平。期间，角膜荧光素钠染色先增加后减少，模型鼠的眼表改变与临床MGD相关干眼患者相似。然而，在急性炎症期给予小鼠睑板腺抗炎处理，睑板腺修复显著减慢。据此，我们猜想急性炎症可能促进睑板腺再生修复。本项目拟对通过睑板腺急性损伤模型的研究，明确急性炎症对睑板腺修复的作用，并尝试对老年睑板腺萎缩小鼠进行治疗，探究其实际治疗作用，对临床睑板腺萎缩的治疗具有重要意义。

The incidence of meibomian gland dysfunction (MGD) increased year by year, which was significantly correlated with age. The occurrence of MGD is directly related to meibomian gland atrophy in middle-aged and elderly people. It is difficult to treat meibomian gland atrophy effectively by existing clinical treatment methods. We found that after acute freezing injury of meibomian gland in mice, the acinar area first decreased, then increased, and finally returned to the normal level. During this period, corneal fluorescein staining first increased and then decreased, and the changes in the ocular surface of the model were similar to those of clinical MGD-related dry eyes. However, the meibomian gland repair was significantly slowed down when the mouse meibomian gland was given anti-inflammatory treatment in the acute inflammatory phase. Therefore, we hypothesized that acute inflammation may promote meibomian gland regeneration and repair. This project intends to clarify the effect of acute inflammation on meibomian gland repair through the study of acute meibomian gland injury model, and try to treat elderly meibomian gland atrophy mice to explore its actual therapeutic effect, which is of great significance for the clinical treatment of meibomian gland atrophy.