The protective mechanisms of glycyrrhizic acid for deoxynivalenol-induced toxicity in rabbit corneal stroma

Objectives This study aimed to investigate the effects and mechanisms of deoxynivalenol (DON) on rabbit corneal stroma cell culture and observe the protective effect of glycyrrhizic acid (GA) against DON-induced damage. Methods Rabbit corneal stromal cells (RCSCs) were isolated and divided into groups: control group (CON), 0.5 mmol/L GA (GA group), 400 ng/mL DON (DON group), and 0.5 mmol/L GA + 400 ng/mL DON (GAD). The effect of GA on RCSCs induced by DON was evaluated using various assays, including CCK-8 assay, Flow cytometry, qPCR, and Western blot. Results DON inhibited RCSCs proliferation, increased apoptosis, and raised the proportion of cells in the S and G2/M phase. It raised reactive oxygen species (ROS) levels and reduced mitochondrial membrane potential (MMP). Additionally, DON upregulated Bax, Caspase-3, inflammatory factors (IL-1α, IL-1β, TNF-α), and matrix metalloproteinases (MMP-1/8), while downregulating tissue inhibitors of matrix metalloproteinases (TIMP-1) and type I collagen. In contrast, GA partially restored RCSCs proliferation and reduced apoptosis, inflammation, and collagen degradation. Conclusions DON can induce toxicity in RCSCs, promoting the expression of inflammatory factors, disrupting the balance between MMP-1/8 and TIMP-1, and promoting type I collagen degradation. Conversely, GA reduces the oxidative stress damage, cell apoptosis, and inflammatory reaction of RCSCs induced by DON, and reduces the degradation of type I collagen.