ArticleScientific reports2025
Exploratory insights into salivary E-cadherin as a non-invasive biomarker in a rat model of diabetes.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
E-cadherin, an adhesion molecule critical for epithelial integrity, may be downregulated by oxidative stress (OS) in diabetes. While serum E-cadherin has been investigated in various conditions, its presence in saliva and potential as a non-invasive biomarker for diabetes remain poorly understood. This study aimed to evaluate salivary E-cadherin levels in streptozotocin (STZ)-induced diabetic rats and examine their relationship with OS markers, assessing the potential of E-cadherin as a non-invasive early diagnostic biomarker for diabetes. Twenty male Wistar rats were randomly assigned to control and diabetic groups. The diabetic model was established by administering a single intraperitoneal injection of 65 mg/kg STZ. Saliva was collected via pilocarpine stimulation, and blood samples were obtained for serum analysis. Salivary and serum E-cadherin levels, alongside serum OS markers including malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were measured. Pearson's correlation assessed relationships between E-cadherin and OS markers. Diabetic rats exhibited significantly lower salivary E-cadherin levels (0.60 ± 0.15 ng/ml) compared to controls (1.21 ± 0.45 ng/ml; p < 0.05). Serum E-cadherin levels were higher than salivary levels in both groups (Control: 18.17 ± 2.23 vs. 1.21 ± 0.45 ng/ml, p < 0.001; Diabetic: 15.64 ± 3.62 vs. 0.60 ± 0.15 ng/ml, p < 0.001), but serum E-cadherin was also reduced in diabetic rats (15.64 ± 3.62 ng/ml) compared to controls (18.17 ± 2.23 ng/ml; p < 0.05). Diabetic rats showed elevated MDA (1.32 ± 0.03 nmol/ml vs. 0.50 ± 0.04 nmol/ml in controls; p < 0.001) and decreased antioxidant markers: GSH (0.76 ± 0.06 vs. 2.55 ± 0.04 µg/ml; p < 0.001), SOD (0.11 ± 0.02 vs. 0.18 ± 0.02 inhibition rate; p < 0.001), and CAT (2.02 ± 0.17 vs. 4.84 ± 0.56 mU/ml; p < 0.001). Furthermore, significant negative correlations were observed between E-cadherin and MDA levels (p < 0.05), while salivary E-cadherin positively correlated with GSH (p < 0.01) and SOD (p < 0.05). This preclinical investigation is the first to show that salivary E-cadherin levels are reduced in diabetic rats and correlate with serum levels, indicating that saliva may reflect systemic changes. Associations with oxidative stress markers suggest that oxidative imbalance contributes to E-cadherin downregulation. These findings provide preliminary evidence for salivary E-cadherin as a promising non-invasive biomarker for early detection and monitoring of diabetes-related epithelial dysfunction. Its translational potential lies in enabling simple, stress-free, and accessible screening approaches that could aid in early diagnosis and disease management in clinical settings.
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