Protective Effect and Mechanism of Hydrotalcite on Aspirin-induced Injury of Human Gastric Mucosal Epithelial Cells / 胃肠病学

ABSTRACT

Background: Long-term use of aspirin can cause varying degrees of gastric mucosal injuries. Hydrotalcite may play a protective role on gastric mucosal injuries through multiple mechanisms. Aims: To investigate the protective effect of hydrotalcite on aspirin-induced gastric mucosal injury and its possible mechanism in an in vitro study. Methods: Human gastric mucosal epithelial cell line GES-1 was selected and divided into three groups normal control group, injury group and protection group. GES-1 cells in the latter two groups were co-cultured with aspirin (9 mmol/L), and cells in the protection group was further treated with hydrotalcite (0.6 mg/mL) after aspirin administration. After culturing for 12 hours, morphology of GES-1 cells was observed by inverted microscope and transmission electron microscope. Cell proliferation and apoptosis were assessed by MTT assay and flow cytometry, respectively. Proteomics was used to identify the differentially expressed proteins between injury group and protection group. Results: Compared with the injury group, GES-1 cells in the protection group remained in a relatively intact structure with higher survival rate and lower apoptosis rate (P<0.05). Proteomics revealed that the expressions of T-complex protein 1 subunit beta (TCP-1β) and thioredoxin-dependent peroxide reductase 3 (PRX3), which were related with protein folding and assembly, cytoskeleton function, and antioxidative stress, were up-regulated in GES-1 cells in the protection group. Conclusions: Hydrotalcite can reduce the aspirin-induced gastric mucosal injury via promoting cell proliferation and inhibiting apoptosis. Improvement of the structure and function of intracellular proteins and antioxidative stress might be implicated in its cytoprotective effect.