The protective mechanisms of glycyrrhizic acid for deoxynivalenol-induced toxicity in rabbit corneal stroma
- Toxicol In Vitro. 2025 Oct:108:106104. doi: 10.1016/j.tiv.2025.106104.
- 1. Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
- 2. Renmin Hospital of Wuhan University, Wuhan, China.
- 3. The Sixth Affiliated Hospital of Jinan University, Dongguan, China. Electronic address: [email protected].
- 4. Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China. Electronic address: [email protected].
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.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Virus Protease