Abstract

Objective

In the current study, we evaluated the ameliorative effect of S-allylcysteine (SAC) against streptozotocin (STZ)-nicotinamide (NAD)-induced diabetic nephropathy (DN) in rats and also an attempt was made to establish the molecular mechanism of SAC.

Methods

DN rats were orally supplemented with SAC (150 mg/kg body weight) for a period of 45 days and the effect of SAC on urinary albumin excretion, metabolic parameters, and tubular injury biomarkers by ELISA, total levels and phosphorylation of MEK1/2, ERK1/2, and RSK2 by western blotting analysis in control and experimental rats were assessed.

Results

From this study, we observed that SAC considerably decreased polydipsia, poly urea, polyphagia, albuminuria and the levels of urinary N-acetyl-beta-D-glucosaminidase, neutrophil gelatinase-associated lipocalin, transforming growth factor-β1 and SAC effectively altered the pathological changes in DN rats. SAC also reserved renal cortical phosphorylation of MEK1/2, ERK1/2 and RSK2.

Conclusion

Hence this study recommended that SAC can successfully protect the DN through regulation of MEK1/2-ERK1/2-RSK2 signalling.

中文翻译：

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S-烯丙基半胱氨酸通过抑制 MEK1/2-ERK1/2-RSK2 信号通路对链脲佐菌素-烟酰胺诱导的糖尿病大鼠糖尿病肾病的影响

摘要

客观的

在目前的研究中，我们评估了 S-烯丙基半胱氨酸 (SAC) 对链脲佐菌素 (STZ)-烟酰胺 (NAD) 诱导的大鼠糖尿病肾病 (DN) 的改善作用，并试图建立 SAC 的分子机制。

方法

DN 大鼠口服补充 SAC（150 mg/kg 体重）45 天，通过 ELISA、MEK1/2 的总水平和磷酸化，SAC 对尿白蛋白排泄、代谢参数和肾小管损伤生物标志物的影响，通过蛋白质印迹分析在对照和实验大鼠中评估 ERK1/2 和 RSK2。

结果

从这项研究中，我们观察到 SAC 显着降低了烦渴、聚脲、多食、蛋白尿和尿 N-乙酰-β-D-氨基葡萄糖苷酶、中性粒细胞明胶酶相关载脂蛋白、转化生长因子-β1 和 SAC 的水平，有效地改变了病理学DN大鼠的变化。SAC 还保留了 MEK1/2、ERK1/2 和 RSK2 的肾皮质磷酸化。

结论

因此，本研究建议 SAC 可以通过调节 MEK1/2-ERK1/2-RSK2 信号成功保护 DN。