The American journal of the medical sciences · 2025
Therapeutic efficacy of scopoletin on oxidative stress and cardiac dysfunction in streptozotocin-induced diabetic rats.
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Alqudah Abdelrahim, Qnais Esam, Gammoh Omar, Bseiso Yousra, Wedyan Mohammed, Shilbayeh Sireen Abdul Rahim, Abudalo Rawan, Oqal Muna, Aljabali Alaa A A
Аннотация
BACKGROUND: Cardiac dysfunction associated with diabetes often arises as a serious condition, primarily driven by persistent oxidative imbalance and chronic inflammation. There are few treatments for such complication and therefore, there is considerable interest in natural compounds such as scopoletin has antioxidative and anti-inflammatory activities. This study investigates how scopoletin may influence disease progression in a rat model of diabetic cardiomyopathy induced by streptozotocin (STZ).
METHODS: Thirty-two male Wistar rats were evenly distributed into four study groups using a randomization protocol: a non-diabetic control, an untreated diabetic group, a diabetic group administered scopoletin, and a diabetic group treated with metformin (Glucophage) as a reference therapy. Post-diabetes induction by streptozotocin, treatments were administered for three weeks, subsequently, malondialdehyde (MDA) concentrations were measured along with, the enzymatic activities of key cardiac antioxidants-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)-were evaluated to assess oxidative defense status. ATPase activities, gene expression (p53 and VCAM-1), and histopathological examinations of heart tissues.
RESULTS: Scopoletin treatment significantly reduced MDA levels by up to 35 %, with p < 0.01 compared to the diabetic control. Antioxidant enzyme activities were notably enhanced, with increases in SOD, CAT, and GPx activities by approximately 50 % (p < 0.01). Cardiac ATPase activities showed marked improvement (p < 0.05), and the expression of p53 and VCAM-1 was effectively downregulated (p < 0.01). Histopathological analysis revealed substantial reductions in myocardial damage, vacuolation, and tissue congestion in scopoletin-treated groups, with the high-dose effects comparable to those observed with metformin (Glucophage).
CONCLUSIONS: Scopoletin demonstrates significant potential in treating diabetic cardiomyopathy. These results encourage further clinical trials to explore scopoletin as a complementary therapy for cardiac complications in diabetic patients.
METHODS: Thirty-two male Wistar rats were evenly distributed into four study groups using a randomization protocol: a non-diabetic control, an untreated diabetic group, a diabetic group administered scopoletin, and a diabetic group treated with metformin (Glucophage) as a reference therapy. Post-diabetes induction by streptozotocin, treatments were administered for three weeks, subsequently, malondialdehyde (MDA) concentrations were measured along with, the enzymatic activities of key cardiac antioxidants-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)-were evaluated to assess oxidative defense status. ATPase activities, gene expression (p53 and VCAM-1), and histopathological examinations of heart tissues.
RESULTS: Scopoletin treatment significantly reduced MDA levels by up to 35 %, with p < 0.01 compared to the diabetic control. Antioxidant enzyme activities were notably enhanced, with increases in SOD, CAT, and GPx activities by approximately 50 % (p < 0.01). Cardiac ATPase activities showed marked improvement (p < 0.05), and the expression of p53 and VCAM-1 was effectively downregulated (p < 0.01). Histopathological analysis revealed substantial reductions in myocardial damage, vacuolation, and tissue congestion in scopoletin-treated groups, with the high-dose effects comparable to those observed with metformin (Glucophage).
CONCLUSIONS: Scopoletin demonstrates significant potential in treating diabetic cardiomyopathy. These results encourage further clinical trials to explore scopoletin as a complementary therapy for cardiac complications in diabetic patients.