Molecular biology reports · 2026
Regulating ferroptosis: the impact of stevia on alleviating liver damage in streptozotocin-induced diabetic rats.
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Amirahmadi Zahra, Raeisi Alireza, Koohpeyma Farhad, Moghadam Delaram, Kiani Roozbeh, Jamshidi Sanaz, Shams Fatemeh, Naeimi Sirous, Dastghaib Sanaz
Аннотация
BACKGROUND: Diabetes-related complications are associated with ferroptosis, an iron-dependent form of cell death characterized by lipid peroxide accumulation and disrupted redox homeostasis. This study investigated the potential protective effects of aquatic Stevia extract against liver damage and ferroptosis in streptozotocin (STZ)-induced diabetic rats.
METHODS: Twenty-four rats were randomly allocated to four groups (n = 6/group): (1) Control, receiving 1 ml water; (2) STZ, receiving STZ (60 mg/kg) and 1 ml water; (3) Stevia, receiving aquatic Stevia extract (400 mg/kg); and (4) Met, receiving metformin (500 mg/kg). After 28 days, serum biochemical parameters, antioxidant status, inflammatory and ferroptosis-related gene expression, TUNEL assay, and liver histopathology were evaluated.
RESULTS: Compared with diabetic controls, Stevia significantly decreased FBS (p < 0.01), ALT (p < 0.05), AST (p < 0.01), IL-6 (p < 0.001), CRP (p < 0.0001), and MDA (p < 0.01), while it increased body weight (p < 0.05), TAC (p < 0.001), and serum GPX, SOD, and CAT (all p < 0.001). Stevia upregulated GPX4 (p < 0.05), FTH1 (p < 0.01), and SLC7 (p < 0.001), while reducing the inflammatory markers NFKβ, TNFα, and IL1β. TUNEL analysis showed reduced apoptotic cells (p < 0.01), with improved liver morphology.
CONCLUSION: These findings suggest that aquatic Stevia extract on diabetic rats through modulation of the ferroptosis pathway, highlighting its potential therapeutic benefits in diabetes-related liver complications.
METHODS: Twenty-four rats were randomly allocated to four groups (n = 6/group): (1) Control, receiving 1 ml water; (2) STZ, receiving STZ (60 mg/kg) and 1 ml water; (3) Stevia, receiving aquatic Stevia extract (400 mg/kg); and (4) Met, receiving metformin (500 mg/kg). After 28 days, serum biochemical parameters, antioxidant status, inflammatory and ferroptosis-related gene expression, TUNEL assay, and liver histopathology were evaluated.
RESULTS: Compared with diabetic controls, Stevia significantly decreased FBS (p < 0.01), ALT (p < 0.05), AST (p < 0.01), IL-6 (p < 0.001), CRP (p < 0.0001), and MDA (p < 0.01), while it increased body weight (p < 0.05), TAC (p < 0.001), and serum GPX, SOD, and CAT (all p < 0.001). Stevia upregulated GPX4 (p < 0.05), FTH1 (p < 0.01), and SLC7 (p < 0.001), while reducing the inflammatory markers NFKβ, TNFα, and IL1β. TUNEL analysis showed reduced apoptotic cells (p < 0.01), with improved liver morphology.
CONCLUSION: These findings suggest that aquatic Stevia extract on diabetic rats through modulation of the ferroptosis pathway, highlighting its potential therapeutic benefits in diabetes-related liver complications.