糖尿病肾病（DN）的发病机制涉及氧化应激和炎症的细胞激活。圣草酚是一种柑橘类黄酮，在各种条件下具有多种药理和保护作用。圣草酚对糖尿病和糖尿病肾病的保护作用研究较少。本研究旨在探讨圣草酚在预防链脲佐菌素引起的雄性大鼠 DN 中的作用，并探讨一些可能的作用机制。大鼠通过腹腔注射单一剂量（65 毫克/公斤）引起糖尿病。纳入五组大鼠（每组 n = 8）作为对照（非糖尿病）、圣草酚（20 mg/kg，口服）、STZ 糖尿病、STZ 圣草酚（20 mg/kg，口服）和 STZ 圣草酚（20 mg/kg，口服）ML385（30 µg/kg，腹腔注射）。分析所有组大鼠的肾脏组织学以及肾功能、肾脏氧化应激和肾脏炎症的一些标志物的水平。在 STZ 治疗的动物中，圣草酚治疗可防止肾小球和肾小管损伤，并减少肾免疫细胞浸润。它还会增加这些糖尿病大鼠的尿肌酐排泄量，并减少尿量和尿白蛋白、单核细胞趋化蛋白 1 (MCP-1)、尿肾损伤分子 1 (KIM-1) 和去氧肾上腺素的水平。此外，圣草酚刺激糖尿病大鼠肾脏中Nrf2的核蛋白积累，并增强超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、血红素加氧酶-1（HO-1）和过氧化氢酶（CAT）的表达。同时，它降低了 NF-κB 的核水平以及白细胞介素 6 (IL-6)、丙二醛 (MDA) 和肿瘤坏死因子-α (TNF-α) 的水平，并减弱了肾 ATP 水平和肾损伤的降低。线粒体过渡孔开放（mtTPT）增加。然而，给予圣草酚并不影响大鼠的体重以及空腹血糖和胰岛素水平，但显着降低了胆固醇、甘油三酯、LDL-c和氧化LDL-c（ox-LDL-c）的血清水平。总之，圣草酚通过激活 Nrf2/NF-κB/抗氧化轴介导的降血脂作用以及伴随的抗氧化和抗炎作用来预防 STZ 诱导的肾病。© 2023 作者。

The pathogenesis of diabetic nephropathy (DN) involves cellular activation of oxidative stress and inflammation. Eriodictyol is a citrus-derived flavonoid with multiple pharmacological and protective effects in various conditions. The protective role of Eriodictyol against diabetes and diabetic nephropathy is less investigated. The current research aimed to explore the role of eriodictyol in protecting against DN prompted by streptozotocin in male rats and investigate some possible mechanisms of action. Diabetes was brought about in rats by an i.p injection of a lone dose (65 mg/kg). Five groups of rats were included (n = 8 each) as control (non-diabetic), eriodictyol (20 mg/kg, orally), STZ-diabetic, STZ + eriodictyol (20 mg/kg, orally), and STZ + eriodictyol (20 mg/kg, orally) + ML385 (30 µg/kg, i.p.). Kidney histology and the levels of some markers of kidney function, renal oxidative stress, and renal inflammation were analyzed in all groups of rats. Treatment with eriodictyol prevented the damage in the renal glomeruli and tubules and reduced renal immune cell infiltration in STZ-treated animals. It also spiked urinary creatinine excretion and reduced urine volume and urinary levels of albumin, monocyte chemoattractant protein 1 (MCP-1), urinary kidney injury molecule-1 (KIM-1), and nephrin in these diabetic rats. In addition, eriodictyol stimulated the nuclear protein accumulation of Nrf2 and boosted the expression of superoxide dismutase (SOD), glutathione (GSH), heme oxygenase-1 (HO-1), and catalase (CAT) in the diabetic rat kidneys. In concomitance, it reduced the nuclear levels of NF-κB and levels of interleukine-6 (IL-6), malondialdehyde (MDA), and tumor necrosis factor-α (TNF-α) and attenuated the reduction in renal ATP levels and the increase in the mitochondria transition pore opening (mtTPT). However, the administration of eriodictyol did not affect rats' body weights and fasting glucose and insulin levels but significantly reduced serum levels of cholesterol, triglycerides, LDL-c, and oxidized LDL-c (ox-LDL-c). In conclusion, eriodictyol prevents STZ-induced nephropathy by a hypolipidemic effect and concomitant antioxidant and anti-inflammatory effects mediated by activating Nrf2/NF-κB/antioxidant axis.© 2023 The Author(s).