Protective effects of Morus alba Linn leaf extract on streptozotocin-induced diabetic nephropathy in mice model
Background: Diabetic nephropathy, a major microvascular complication of type 2 diabetes, arises from chronic hyperglycemia-induced renal dysfunction. Current therapies have limited efficacy in halting its progression. Purpose: The aim of this study was to evaluate the nephroprotective potential of M...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-08-01
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| Series: | Phytomedicine Plus |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2667031325000910 |
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| Summary: | Background: Diabetic nephropathy, a major microvascular complication of type 2 diabetes, arises from chronic hyperglycemia-induced renal dysfunction. Current therapies have limited efficacy in halting its progression. Purpose: The aim of this study was to evaluate the nephroprotective potential of Morus alba Linn leaf extract (MAE) against streptozotocin-induced diabetic nephropathy in a mouse model. Methods: Diabetic nephropathy was induced in Swiss mice using multiple low-dose streptozotocin intraperitoneal injections. Mice received MAE (820.8 or 2462.4 mg/kg) or dapagliflozin (1 mg/kg) orally for 28 days. Results: Morus alba Linn leaf extract reduced fasting blood glucose (FBG), triglycerides, total cholesterol, lipoprotein combine index (LCI), and urinary albumin-creatinine ratio (UACR) while increasing creatinine clearance (Ccr) compared to diabetic controls. Specifically, after 28 days of treatment, MAE at 820.8 mg/kg reduced FBG from 16.56 ± 3.90 mmol/L in diabetic controls to 9.69 ± 2.15 mmol/L (p < 0.01), and at 2462.4 mg/kg to 12.51 ± 4.17 mmol/L (p < 0.05). Additionally, Ccr increased from 16.80 ± 10.80 µl/min in diabetic controls to 41.84 ± 27.02 µl/min with low-dose MAE (p < 0.05) and 39.72 ± 15.54 µl/min with high-dose MAE (p < 0.01). Histopathological analysis revealed reduced glomerulosclerosis, tubular degeneration, and pancreatic islet damage in MAE-treated groups. However, MAE did not improve glucose tolerance in the oral glucose tolerance test, and changes in renal malondialdehyde (MDA) and tumor necrosis factor-α (TNF-α) were not significant, suggesting limited effects on dynamic glucose handling and oxidative/inflammatory pathways. A trend toward increased glutathione (GSH) was observed. Conclusions: These findings suggest MAE as a promising candidate for managing diabetic nephropathy, but further mechanistic and clinical studies are needed to validate its therapeutic potential. |
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| ISSN: | 2667-0313 |