Related Experiment Video
Updated: Jul 30, 2025

Author Spotlight: Exploring Huotan Jiedu Tongluo Decoction as an Antihypertensive Drug
Published on: May 17, 2024
Renal herb formula protects against hyperuricemic nephropathy by inhibiting apoptosis and inflammation
Guo-Yi Tang1, Sha Li1, Yu Xu1
1School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 999077 Hong Kong S.A.R., P.R. China.
Background:
Hyperuricemic nephropathy may be induced by the elevation and accumulation of uric acid in kidney after hyperuricemia, which leads to kidney residential cells apoptosis and inflammation. Renal herb formula (RHF) is a self-designed formula based on traditional Chinese medicine theory and clinical practice in kidney disease treatment. In the literature available currently, there is not yet research article reporting the reno-protective effect of RHF against hyperuricemic nephropathy.
Purpose:
This study was performed to analyze the bioactive compound profiles of RHF, evaluate its protective effects against hyperuricemic nephropathy, and investigate the mechanisms of actions regarding apoptosis and inflammation.
Methods:
Ultra-performance liquid chromatography with a diode-array detector was applied to establish fingerprint and chemical composition of RHF. Potassium oxonate was used to induce hyperuricemic nephropathy in mice, and uric acid was used to stimulate apoptosis and inflammatory response in HK-2 cells, while the mice and cells were treated with RHF to explore its reno-protective effects and mechanisms.
Results:
It was found that chlorogenic acid, neochlorogenic acid, cryptochlorogenic acid, and isochlorogenic acid A-C may be the characteristic components of RHF. RHF treatment could improve kidney functions in mice with hyperuricemic nephropathies, such as decreasing urine protein, uric acid, and creatinine and serum uric acid, creatinine, and urea nitrogen. Histopathological observations showed that RHF treatment ameliorated kidney glomerular hypotrophy, tubular damage, and inflammatory infiltration. Mechanism studies revealed that RHF inhibited kidney residential cell apoptosis and inflammatory response by targeting the p53-associated intrinsic apoptosis pathway and NF-κB-mediated inflammatory pathway.
Conclusion:
Taken together, it could be concluded that RHF exerted reno-protective effects against hyperuricemic nephropathy through reducing apoptosis and inflammation. RHF and the bioactive compounds chlorogenic acid analogs as promising candidates may be developed into novel and effective drugs for hyperuricemic nephropathy treatment and management.
More Related Videos
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
06:46Author Spotlight: Understanding the Effect of Herbal-Cake-Separated Moxibustion in Rats with Renal Faliure
Published on: December 22, 2023
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antihypertensive Drugs: Action of Diuretics
Antihypertensive Drugs: Direct Renin Inhibitors
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Urinary Tract Calculi IV: Nutrition Therapy and Prevention
Acute Kidney Injury VI: Nursing Management