桑叶提取物对链脲佐菌素致糖尿病肾病模型小鼠的保护作用

Q3 Pharmacology, Toxicology and Pharmaceutics

Phytomedicine Plus Pub Date : 2025-05-19 DOI:10.1016/j.phyplu.2025.100819

Ngoc Kim Nguyen , Ha Thu Thi Nguyen , Thanh Phuong Mai , Quang Vinh Trinh , Nghia Trong Duong , Phong Xuan Pham , Van Anh Thi Pham

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引用次数: 0

摘要

背景：糖尿病肾病是2型糖尿病的主要微血管并发症，由慢性高血糖引起的肾功能障碍引起。目前的治疗方法在阻止其进展方面效果有限。目的观察桑叶提取物（MAE）对链脲佐菌素诱导的糖尿病肾病的肾保护作用。方法采用低剂量链脲佐菌素多次腹腔注射诱导瑞士小鼠糖尿病肾病。小鼠口服MAE（820.8或2462.4 mg/kg）或dapagliflozin (1 mg/kg)，持续28天。结果与糖尿病对照组相比，桑叶提取物可降低空腹血糖（FBG）、甘油三酯、总胆固醇、脂蛋白联合指数（LCI）和尿白蛋白-肌酐比（UACR），提高肌酐清除率（Ccr）。具体来说，治疗28天后，820.8 mg/kg的MAE使糖尿病对照组的空腹血糖从16.56±3.90 mmol/L降至9.69±2.15 mmol/L (p <；从2462.4 mg/kg降至12.51±4.17 mmol/L (p <；0.05)。此外，低剂量MAE组的Ccr从糖尿病对照组的16.80±10.80µl/min增加到41.84±27.02µl/min (p <；高剂量MAE组为39.72±15.54µl/min (p <；0.01)。组织病理学分析显示，mae治疗组的肾小球硬化、小管变性和胰岛损伤减轻。然而，在口服糖耐量试验中，MAE并没有改善糖耐量，肾脏丙二醛（MDA）和肿瘤坏死因子-α (TNF-α)的变化也不显著，表明MAE对动态葡萄糖处理和氧化/炎症途径的影响有限。观察到谷胱甘肽（GSH）增加的趋势。结论MAE是治疗糖尿病肾病的一个有希望的候选药物，但需要进一步的机制和临床研究来验证其治疗潜力。

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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 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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