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Updated: Mar 1, 2026
Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
Published on: April 25, 2025
Arctigenin suppresses renal interstitial fibrosis in a rat model of obstructive nephropathy
Ao Li1, Xiaoxun Zhang2, Mao Shu2
1College of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, China; State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau 999078, China.
Background:
Renal tubulointerstitial fibrosis (TIF) is commonly the final result of a variety of progressive injuries and leads to end-stage renal disease. There are few therapeutic agents currently available for retarding the development of renal TIF.
Purpose:
The aim of the present study is to evaluate the role of arctigenin (ATG), a lignan component derived from dried burdock (Arctium lappa L.) fruits, in protecting the kidney against injury by unilateral ureteral obstruction (UUO) in rats.
Methods:
Rats were subjected to UUO and then administered with vehicle, ATG (1 and 3mg/kg/d), or losartan (20mg/kg/d) for 11 consecutive days. The renoprotective effects of ATG were evaluated by histological examination and multiple biochemical assays.
Results:
Our results suggest that ATG significantly protected the kidney from injury by reducing tubular dilatation, epithelial atrophy, collagen deposition, and tubulointerstitial compartment expansion. ATG administration dramatically decreased macrophage (CD68-positive cell) infiltration. Meanwhile, ATG down-regulated the mRNA levels of pro-inflammatory chemokine monocyte chemoattractant protein-1 (MCP-1) and cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon-γ (IFN-γ), in the obstructed kidneys. This was associated with decreased activation of nuclear factor κB (NF-κB). ATG attenuated UUO-induced oxidative stress by increasing the activity of renal manganese superoxide dismutase (SOD2), leading to reduced levels of lipid peroxidation. Furthermore, ATG inhibited the epithelial-mesenchymal transition (EMT) of renal tubules by reducing the abundance of transforming growth factor-β1 (TGF-β1) and its type I receptor, suppressing Smad2/3 phosphorylation and nuclear translocation, and up-regulating Smad7 expression. Notably, the efficacy of ATG in renal protection was comparable or even superior to losartan.
Conclusion:
ATG could protect the kidney from UUO-induced injury and fibrogenesis by suppressing inflammation, oxidative stress, and tubular EMT, thus supporting the potential role of ATG in renal fibrosis treatment.
Insights
Arctigenin (ATG) protects kidneys from injury by reducing inflammation, oxidative stress, and epithelial-mesenchymal transition (EMT). This natural compound shows potential for treating renal fibrosis.
Area of Science:
- Nephrology
- Pharmacology
- Natural Products Chemistry
Background:
- Renal tubulointerstitial fibrosis (TIF) is a common outcome of progressive kidney injuries, often leading to end-stage renal disease.
- Limited therapeutic options exist to slow the progression of renal TIF.
Purpose of the Study:
- To investigate the protective effects of arctigenin (ATG), a lignan from Arctium lappa, against kidney injury induced by unilateral ureteral obstruction (UUO) in a rat model.
- To evaluate ATG's potential as a therapeutic agent for renal fibrosis.
Main Methods:
- Rats underwent UUO and were treated with vehicle, ATG (1 and 3 mg/kg/d), or losartan (20 mg/kg/d) for 11 days.
- Renoprotective effects were assessed via histological examination and biochemical assays, including analysis of inflammatory markers, oxidative stress, and epithelial-mesenchymal transition (EMT).
Main Results:
- ATG significantly reduced kidney injury markers, including tubular dilatation, atrophy, collagen deposition, and interstitial expansion.
- ATG decreased macrophage infiltration and suppressed pro-inflammatory cytokine (MCP-1, TNF-α, IL-1β, IFN-γ) mRNA levels by inhibiting NF-κB activation.
- ATG attenuated oxidative stress by enhancing SOD2 activity and reducing lipid peroxidation, while also inhibiting UUO-induced tubular EMT by modulating TGF-β1/Smad signaling pathways.
Conclusions:
- Arctigenin demonstrates significant renoprotective effects against UUO-induced injury and fibrosis in rats.
- ATG achieves this by suppressing inflammation, oxidative stress, and tubular EMT, highlighting its therapeutic potential for renal fibrosis.
- The efficacy of ATG was comparable or superior to losartan, suggesting its promise as a novel treatment strategy.
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