Dry eye (DE) is a chronic, multifactorial ocular surface disease associated with visual disturbance, tear film instability, hyperosmolarity, ocular surface inflammation and damage. Effective intervention is necessary to control this disease. In this study we topically applied α-melanocyte stimulating hormone (α-MSH) on the ocular surface of scopolamine-induced DE rats and found that it promoted tear secretion, reduced tear breakup time and fluorescein sodium staining and increased the number of conjunctival goblet cells. To investigate the mechanism, protein array was conducted, which showed that α-MSH exerted its effects via epithelial growth factor receptor (EGFR) in the JAK-STAT signaling pathway. Furthermore, in vitro experiments showed that α-MSH protected human corneal epithelial cells (hCECs) by maintaining their migration ability and viability and decreasing apoptosis. However, blockade of EGFR abolished these protective effects. Moreover, α-MSH decreased the level of autophagy in benzalkonium chloride (BAC)-stressed hCECs via EGFR. These results demonstrated that α-MSH ameliorated lesions and restored ocular surface functions by upregulating EGFR expression.

干眼症 (DE) 是一种慢性、多因素的眼表疾病，与视觉障碍、泪膜不稳定、高渗性、眼表炎症和损伤相关。需要有效的干预来控制这种疾病。在本研究中，我们在东莨菪碱诱导的 DE 大鼠眼表局部应用 α-促黑素细胞激素（α-MSH），发现它促进泪液分泌，减少泪液破裂时间和荧光素钠染色，并增加结膜杯状细胞的数量. 为了研究其机制，进行了蛋白质阵列，表明α-MSH通过JAK-STAT信号通路中的上皮生长因子受体（EGFR）发挥作用。此外，体外实验表明，α-MSH 通过维持人角膜上皮细胞 (hCEC) 的迁移能力和活力并减少细胞凋亡来保护它们。然而，EGFR 的阻断消除了这些保护作用。此外，α-MSH 通过 EGFR 降低了苯扎氯铵 (BAC) 应激的 hCEC 中的自噬水平。这些结果表明，α-MSH 通过上调 EGFR 表达来改善病变并恢复眼表功能。