中国临床药理学与治疗学 ›› 2026, Vol. 31 ›› Issue (7): 928-936.doi: 10.12092/j.issn.1009-2501.2026.07.009
郑丽萍1,2,3(
), 朱晗1,2,3, 赵克勤2, 黄勇3,*(
), 刘鹏2,*(
)
收稿日期:2025-09-19
修回日期:2025-10-12
出版日期:2026-07-26
发布日期:2026-08-04
通讯作者:
黄勇,刘鹏
E-mail:zlp18307007805@163.com;huangy870613@126.com;drliupeng@sina.cn
作者简介:郑丽萍,女,在读研究生,研究方向:中医药防治慢性肾脏病的基础及临床研究。E-mail:基金资助:
Liping ZHENG1,2,3(
), Han ZHU1,2,3, Keqin ZHAO2, Yong HUANG3,*(
), Peng LIU2,*(
)
Received:2025-09-19
Revised:2025-10-12
Online:2026-07-26
Published:2026-08-04
Contact:
Yong HUANG,Peng LIU
E-mail:zlp18307007805@163.com;huangy870613@126.com;drliupeng@sina.cn
摘要:
糖尿病肾病(diabetic kidney disease,DKD)是一种继发于糖尿病的常见微血管并发症。其发病率呈现逐年增加的趋势,严重威胁糖尿病患者的预后和生活质量。目前临床上对于DKD的治疗选择有限,难以有效阻止其进展。在DKD复杂的病理生理机制中,脂代谢紊乱扮演着重要角色,不仅促进肾内脂质沉积,还通过脂毒性加速肾脏损伤进程。近年来,中草药因其在改善DKD脂代谢紊乱方面具有显著效果而备受关注。黄芪是治疗DKD的常用中草药,在DKD的治疗中表现出显著的肾脏保护作用。黄芪富含黄芪甲苷Ⅳ、芒柄花素、槲皮素、山奈酚等活性成分,在改善DKD脂代谢紊乱方面展现出独特优势,其不仅可以有效改善脂代谢异常,还可以减少肾脏脂质沉积。本文系统综述了黄芪活性成分改善DKD脂代谢紊乱的作用研究进展,为临床治疗DKD策略提供理论依据。
中图分类号:
郑丽萍, 朱晗, 赵克勤, 黄勇, 刘鹏. 黄芪活性成分改善糖尿病肾病脂代谢紊乱的研究进展[J]. 中国临床药理学与治疗学, 2026, 31(7): 928-936.
Liping ZHENG, Han ZHU, Keqin ZHAO, Yong HUANG, Peng LIU. Research progress of active components of Astragalus membranaceus in improving lipid metabolism disorder of diabetic kidney disease[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(7): 928-936.
| Active ingredient | Dosage | Time | Model | Signal pathways and targets | Changes of blood lipid index | Reference |
| Astragaloside Ⅳ | 20, 40, 80 mg/kg | 12 W | HFD/STZ rats HK-2 cells | CD36/ROS/NLRP3 | TG↓, TC↓, LDL-C↓, BUN↓, Scr↓, UACR↓ | [ |
| 40, 80 mg/kg | 12 W | HFD/STZ rats podocytes | Klotho/ NF-κB/NLRP3 | TG↓, TC↓, SCr↓, BUN↓, UACR↓ | [ | |
| 25, 50, 100 mg/kg | 12 W | HFD/STZ mice HK-2 cells | HIF-1α/HMOX1 | TG↓, LDL-C↓, BG↓ | [ | |
| Formononetin | 25, 50 mg/kg | 8 W | db/db mice | Smad3 | TG↓, TC↓, FBG↓, FINS↓, IRI↓, ISI↑ | [ |
| 25, 50 mg/kg | 8 W | db/db mice GMCs | Sirt1/Nrf2/ARE | TG↓, TC↓, SCr↓, BUN↓, ACR↓ | [ | |
| Quercetin | 50, 100 mg/kg | 10 W | db/db mice | SCAP-SREBP2-LDLr/ HMGCR | TG↓, TC↓, LDL-C↓, Crea↓, Urea↓, HDL-C↑ | [ |
| 50, 100 mg/kg | 12 W | db/db mice | TGF-β1/Smad | TG↓, BUN↓, Ccr↓ | [ | |
| 50 mg/kg | 5 W | HFD/STZ rats | Sirt1/Nrf2/HO-1 | TG↓, LDL-C↓, HDL-C↑ | [ | |
| Kaempferol | 50, 100 mg/kg | 12 W | db/db mice | AMPK/mTOR | TC↓, LDL-C↓, SCr↓, UACR↓, FBG↓ | [ |
表 1
Table 1 The potential renal protective effect of active components of Astragalus membranaceus
| Active ingredient | Dosage | Time | Model | Signal pathways and targets | Changes of blood lipid index | Reference |
| Astragaloside Ⅳ | 20, 40, 80 mg/kg | 12 W | HFD/STZ rats HK-2 cells | CD36/ROS/NLRP3 | TG↓, TC↓, LDL-C↓, BUN↓, Scr↓, UACR↓ | [ |
| 40, 80 mg/kg | 12 W | HFD/STZ rats podocytes | Klotho/ NF-κB/NLRP3 | TG↓, TC↓, SCr↓, BUN↓, UACR↓ | [ | |
| 25, 50, 100 mg/kg | 12 W | HFD/STZ mice HK-2 cells | HIF-1α/HMOX1 | TG↓, LDL-C↓, BG↓ | [ | |
| Formononetin | 25, 50 mg/kg | 8 W | db/db mice | Smad3 | TG↓, TC↓, FBG↓, FINS↓, IRI↓, ISI↑ | [ |
| 25, 50 mg/kg | 8 W | db/db mice GMCs | Sirt1/Nrf2/ARE | TG↓, TC↓, SCr↓, BUN↓, ACR↓ | [ | |
| Quercetin | 50, 100 mg/kg | 10 W | db/db mice | SCAP-SREBP2-LDLr/ HMGCR | TG↓, TC↓, LDL-C↓, Crea↓, Urea↓, HDL-C↑ | [ |
| 50, 100 mg/kg | 12 W | db/db mice | TGF-β1/Smad | TG↓, BUN↓, Ccr↓ | [ | |
| 50 mg/kg | 5 W | HFD/STZ rats | Sirt1/Nrf2/HO-1 | TG↓, LDL-C↓, HDL-C↑ | [ | |
| Kaempferol | 50, 100 mg/kg | 12 W | db/db mice | AMPK/mTOR | TC↓, LDL-C↓, SCr↓, UACR↓, FBG↓ | [ |
图 1
Fig.1 The mechanism of Astragalus membranaceus active ingredients improving lipid metabolism disorder in diabetic kidney disease CD36: cluster of differentiation 36; ROS: reactive oxygen species; NLRP3: NOD-like receptor family pyrin domain containing 3; NF-κB: nuclear factor kappa β; HIF-1α: hypoxia-inducible factor 1-alpha; HO-1: heme oxygenase-1; Nrf2: nuclear factor erythroid 2-related factor 2; ARE: antioxidant response element; LDLr: low-density lipoprotein receptors; SREBP2: sterol regulatory element-binding protein 2; SCAP: SREBP cleavage-activating protein; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase; TGF-β1: transforming growth factor-beta 1; Sirt1: sirtuin-1; AMPK: AMP-activated protein kinase; mTOR: mechanistic target of rapamycin.
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