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1.河南中医药大学第二临床医学院,郑州;450011
2.河南省中医院(河南中医药大学第二附属医院)肾病科,郑州 450002
硕士研究生。研究方向:中西医结合防治肾脏病。 E-mail:15515673725@163.com
副主任医师,硕士生导师,博士。研究方向:中西医结合防治肾脏病。E-mail:doctorpang@aliyun.com
收稿:2025-09-01,
修回:2025-11-08,
录用:2025-11-10,
纸质出版:2025-12-15
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牛娣,陈瑞芳,黄新蒙,等.地黄在糖尿病肾病中的药理作用机制研究进展 [J].中国药房,2025,36(23):2995-3000.
NIU Di,CHEN Ruifang,HUANG Xinmeng,et al.Research progress on the pharmacological mechanism of Rehmannia glutinosa in diabetic kidney disease[J].ZHONGGUO YAOFANG,2025,36(23):2995-3000.
牛娣,陈瑞芳,黄新蒙,等.地黄在糖尿病肾病中的药理作用机制研究进展 [J].中国药房,2025,36(23):2995-3000. DOI: 10.6039/j.issn.1001-0408.2025.23.20.
NIU Di,CHEN Ruifang,HUANG Xinmeng,et al.Research progress on the pharmacological mechanism of Rehmannia glutinosa in diabetic kidney disease[J].ZHONGGUO YAOFANG,2025,36(23):2995-3000. DOI: 10.6039/j.issn.1001-0408.2025.23.20.
糖尿病肾病(DKD)是糖尿病最常见且最严重的微血管并发症之一,目前尚缺乏有效延缓其进展的治疗手段。中医药治疗DKD历史悠久,具有独特优势。地黄作为传统中药,在临床和现代药理学研究中显示出对DKD的治疗潜力。本文整合地黄在DKD中药理作用机制的相关研究后发现,地黄主要活性成分(梓醇、地黄苷D、桃叶珊瑚苷、毛蕊花糖苷、红景天苷、松果菊苷、地黄多糖)、地黄提取物及相关中药复方(六味地黄丸、参芪地黄汤、肾气丸等)可通过干预晚期糖基化终末产物(AGE)/AGE受体、核因子
κB、转化生长因子β
1
/Smad等多条通路,发挥改善DKD代谢紊乱与氧化应激,抑制肾脏炎症与纤维化进程,调控凋亡、铁死亡等细胞死亡方式与细胞自噬,并重塑肠道菌群的多重作用,改善理化指标及肾脏组织病理损伤,进而延缓DKD进展。
Diabetic kidney disease (DKD) is one of the most common and harmful microvascular complications of diabetes, and there is currently a lack of effective treatment methods to delay its progression. Traditional Chinese medicine has a long history of treating DKD and offers unique advantages. As a traditional Chinese medicine,
Rehmannia glutinosa
has shown potential in the treatment of DKD in clinical and modern pharmacological research. After integrating relevant research on the pharmacological mechanism of
R. glutinosa
in treating DKD, it has been found that the main active components of
R. glutinosa
, such as catalpol, rehmannioside D, aucubin, verbascoside, salidroside, echinacoside and
R. glutinosa
polysaccharides, along with its extracts and compounds (such as Liuwei dihuang pills, Shenqi dihuang decoction, and Shenqi pills), can exert multiple effects by intervening in various signaling pathways, including advanced glycation end product (AGE)/receptor for AGE, nuclear factor kappa-B (NF-κB), and transforming growth factor-β
1
(TGF-β
1
)/Smads. These effects include ameliorating metabolic disorders and oxidative stress in DKD, inhibiting the processes of renal inflammation and fibrosis, regulating cell death modalities including apoptosis and ferroptosis, as well as autophagy, and reshaping the gut microbiota. Consequently, it can improve physical and chemical indices and renal tissue pathological damage, thus delaying the progression of DKD.
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