Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes

Abstract Background: Premature rupture of membranes is an important cause of preterm birth and its associated high infant mortality and morbidity, and is an important public health problem worldwide, but the mechanism is unknown, and clinical treatment is currently mainly conservative, with a lack of effective interventions. We compared the differential metabolites in vaginal secretions between patients with preterm premature rupture of membranes and those with normal pregnancies and screened for the protective substance N-acetyl-d-galactosamine (GalNAc), an important ligand for galectin, which has several biological activities such as anti-inflammatory, antioxidant and in vitro wound healing properties. Methods: We evaluated the inflammatory response, oxidative stress, proliferation migration, EMT and ECM remodelling of human amniotic epithelial cells (WISH) by ELISA, ROS, transwell, scratch and CCK-8 assays, and examined the expression of PCNA and AKT by Western Blot. Results: The results showed that GalNAc enhanced galectin production and inhibited cellular inflammation and oxidative stress, promoted cellular EMT and migration, and altered ECM composition. In addition, GalNAc reduced the total and phosphorylated protein levels of AKT enhancing the pro-cell migration ability of GalNAc to stimulate wound healing. Conclusions: The results showed that GalNAc enhanced galectin production and inhibited cellular inflammation and oxidative stress, promoted cellular EMT and migration, synthesized GAG and altered ECM composition. The GalNAc-galectin pathway may provide a theoretical basis and a new target for the prevention and treatment of premature rupture of membranes. This study provides a theoretical basis and a new target for the prevention and treatment of premature rupture of membranes.