Abstract

This study examined the protective effect of Kaempferol against streptozotocin-induced diabetic nephropathy (DN) in rats and studies the underlying mechanisms. Rats were divided into 4 groups as control, control + Kaempferol, STZ, and STZ + Kaempferol. All treatments were conducted for 8 weeks daily after the induction of diabetes. Kaempferol prevented STZ-induced weight and food loss and attenuated renal damage and the alterations in all biochemical related parameters. Concomitantly, Kaempferol reduced renal levels of TNF-α and IL-6, cleaved caspase-3, p38, and Bax, suppressing JNK phosphorylation and NF-κB p65 transactivation, and upregulation of Bcl-2. In both control and STZ-diabetic rats, Kaempferol reduced fasting glucose levels, increased fasting insulin levels and HOMA-β, reduced the levels of ROS and MDA, stimulated SOD and GSH levels, and increased the expression of Nrf2 and HO-1. In conclusion, Kaempferol prevents STZ-induced diabetic nephropathy, mainly, by antioxidant potential, mediated by the upregulation of the Nrf-2/HO-1 axis.

摘要

本研究检查了山奈酚对链脲佐菌素诱导的大鼠糖尿病肾病 (DN) 的保护作用，并研究了其潜在机制。将大鼠分为4组：对照组、对照组+山奈酚、STZ和STZ+山奈酚。所有治疗均在诱发糖尿病后每天进行8周。山奈酚可防止 STZ 引起的体重和食物损失，并减轻肾损伤和所有生化相关参数的变化。同时，山奈酚降低肾脏中 TNF-α 和 IL-6、裂解 caspase-3、p38 和 Bax 的水平，抑制 JNK 磷酸化和 NF-κB p65 反式激活，以及 Bcl-2 的上调。在对照和 STZ 糖尿病大鼠中，山奈酚降低了空腹血糖水平，增加了空腹胰岛素水平和 HOMA-β，降低了 ROS 和 MDA 水平，刺激了 SOD 和 GSH 水平，并增加了 Nrf2 和 HO-1 的表达。总之，山奈酚主要通过 Nrf-2/HO-1 轴上调介导的抗氧化潜力来预防 STZ 诱导的糖尿病肾病。