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牛蒡低聚果糖通过调节Nrf2信号通路对小鼠糖尿病肾病起到保护作用。

Burdock Fructooligosaccharide Protects Against Diabetic Nephropathy in Mice by Regulating Nrf2 Signaling.

作者信息

Zhu Lei, Ding Mengru, Liu Lina, Yuan Pingchuan, Shao Taili, Liu Chunyan, Xi Chuanhu, Han Jun, Zhou Yuyan, Zhang Donglin, Wang Guodong

机构信息

School of Pharmacy, Wannan Medical College, Wuhu, China.

Anhui Provincial Engineering Research Center for Polysaccharide Drugs, Anhui Provincial Engineering Laboratory for Screening and Re-evaluation of Active Compounds of Herbal Medicines in Southern Anhui, Anhui Innovative Center for Drug Basic Research of Metabolic Diseases, Wuhu, China.

出版信息

Pharmacol Res Perspect. 2025 Jun;13(3):e70094. doi: 10.1002/prp2.70094.

Abstract

Diabetic nephropathy (DN) is a common complication of diabetes mellitus, with oxidative stress playing a critical role in its development. Burdock fructooligosaccharide (BFO), a major compound in Burdock, exhibits antioxidative effects. However, its mechanisms of action and effects on diabetic nephropathy are not clear enough. This study aims to explore the mechanisms of BFO and its impact on streptozotocin-induced diabetic nephropathy in mice. Male C57BL/6J mice were randomly divided into normal control, DN, and BFO groups. Relevant serum biochemical parameters were detected using kits. Renal injury was evaluated through fluorescence microscopy, histopathology, and transmission electron microscopy. Nrf2/HO-1 signaling was analyzed via quantitative real-time PCR, western blotting, and immunohistochemistry. In DN mice, BFO significantly reduced fasting blood glucose, kidney index, urine protein, serum creatinine, blood urea nitrogen, total cholesterol, triglyceride, and low-density lipoprotein cholesterol, while significantly increasing high-density lipoprotein, SOD, and CAT levels. Additionally, BFO protected against streptozotocin-induced renal injury, restored podocyte function, increased both mRNA and protein expression of Nrf2, HO-1, and Bcl-2, and decreased those of Bax. In conclusion, BFO can be used to treat streptozotocin-induced renal injury in mice and is a promising candidate for diabetic nephropathy treatment.

摘要

糖尿病肾病(DN)是糖尿病的常见并发症,氧化应激在其发展过程中起关键作用。牛蒡低聚果糖(BFO)是牛蒡中的主要化合物,具有抗氧化作用。然而,其作用机制以及对糖尿病肾病的影响尚不够明确。本研究旨在探讨BFO对链脲佐菌素诱导的小鼠糖尿病肾病的作用机制及其影响。将雄性C57BL/6J小鼠随机分为正常对照组、糖尿病肾病组和BFO组。使用试剂盒检测相关血清生化参数。通过荧光显微镜、组织病理学和透射电子显微镜评估肾脏损伤。通过定量实时PCR、蛋白质免疫印迹法和免疫组织化学分析Nrf2/HO-1信号通路。在糖尿病肾病小鼠中,BFO显著降低空腹血糖、肾脏指数、尿蛋白、血清肌酐、血尿素氮、总胆固醇、甘油三酯和低密度脂蛋白胆固醇水平,同时显著提高高密度脂蛋白、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)水平。此外,BFO可预防链脲佐菌素诱导的肾损伤,恢复足细胞功能,增加Nrf2、HO-1和Bcl-2的mRNA和蛋白表达,并降低Bax的表达。总之,BFO可用于治疗链脲佐菌素诱导的小鼠肾损伤,是治疗糖尿病肾病的有前景的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1f8/12015130/8879212e74fb/PRP2-13-e70094-g006.jpg

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