Exploring the effect of chlorogenic acid on oxidative stress and autophagy in dry eye mice via the AMPK/ULK1 pathway.

Dry eye disease (DED) is closely associated with oxidative stress (OS); its high prevalence and the limitations of current treatments highlight the need for highly effective antioxidants. Chlorogenic acid (CGA) can upregulate the activity of antioxidant enzymes, hinder the process of lipid peroxidation, and exert potent antioxidant effects. In this study, we established an OS-induced DED mouse model to investigate the protective effect and mechanism of CGA against OS-induced DED. Three aspects were examined: oxidative damage, apoptosis, and autophagy. The results demonstrated that CGA improved ocular surface signs in DED mice, decreased inflammatory responses in the meibomian gland (MG), downregulated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), inhibited apoptosis and autophagy, and regulated proteins related to the AMPK (AMP-activated protein kinase)/ULK1 (UNC-51-like Kinase 1) signaling pathway in the MG of DED mice. These findings suggest that CGA can attenuate oxidative damage and inhibit related apoptosis and autophagy in the MG of DED mice by affecting the expression of proteins related to the AMPK/ULK1 signaling pathway.