Related Experiment Video
Updated: May 30, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
Preventive effects and mechanisms of rhein on renal interstitial fibrosis in obstructive nephropathy
Dongyuan He1, Li Lee, Junwei Yang
1First Clinical Medical College of Nanjing Medical University, Nanjing 210029, P. R. China.
Abstract:
Renal interstitial fibrosis is a common outcome of a variety of chronic renal diseases. Here we evaluated the therapeutic efficacy of rhein on renal interstitial fibrosis induced by unilateral ureteral obstruction (UUO) and investigated the potential mechanisms. Mice underwent UUO, followed by orally administrated rhein (150 mg/kg/d) or control vehicle. Renal interstitial injury and the degree of fibrosis were evaluated by pathological staining and Western blot. The possible mechanisms were studied by Western blot, indirect immune-fluorescence and enzyme-linked immunosorbent assay. Our results showed that rhein therapy markedly ameliorated renal interstitial fibrotic lesions, reduced α-smooth muscle actin (α-SMA) expression, attenuated deposition of fibronectin (FN). Rhein also suppressed transforming growth factor-β1 (TGF-β1) and its type I receptor expression in obstructed kidneys. In vitro, rhein abolished the α-SMA and fibronectin expression of rat kidney interstitial fibroblasts cells (NRK-49F) induced by TGF-β1. These observations strongly suggest that rhein is a potent inhibitor of renal interstitial fibrosis, and its therapeutic mechanism is, at least in part, blocking interstitial fibroblasts cells activation.
Insights
Rhein effectively treats kidney fibrosis by reducing scarring and blocking the activation of kidney cells. This study shows rhein
Area of Science:
- Nephrology
- Pharmacology
- Cell Biology
Background:
- Renal interstitial fibrosis is a significant complication of chronic kidney diseases.
- Unilateral ureteral obstruction (UUO) is a common model to study kidney fibrosis.
- Identifying effective therapeutic agents for renal fibrosis is crucial.
Purpose of the Study:
- To evaluate the therapeutic potential of rhein against renal interstitial fibrosis induced by UUO.
- To elucidate the underlying mechanisms of rhein's action in inhibiting fibrosis.
Main Methods:
- Mice underwent UUO and were treated with rhein or a control vehicle.
- Pathological staining and Western blot were used to assess renal injury and fibrosis.
- Western blot, immune-fluorescence, and ELISA were employed to investigate molecular mechanisms.
- In vitro studies used rat kidney interstitial fibroblast cells (NRK-49F) treated with TGF-β1.
Main Results:
- Rhein treatment significantly reduced renal interstitial fibrotic lesions and injury.
- Rhein decreased the expression of alpha-smooth muscle actin (α-SMA) and fibronectin (FN).
- Rhein suppressed transforming growth factor-β1 (TGF-β1) and its type I receptor in obstructed kidneys.
- In vitro, rhein inhibited TGF-β1-induced α-SMA and fibronectin expression in fibroblasts.
Conclusions:
- Rhein demonstrates potent therapeutic efficacy in ameliorating established renal interstitial fibrosis.
- Rhein's mechanism involves inhibiting interstitial fibroblast activation, partly by suppressing the TGF-β1 signaling pathway.
- Rhein represents a promising therapeutic candidate for treating chronic kidney diseases characterized by fibrosis.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antihypertensive Drugs: Direct Renin Inhibitors
Acute Kidney Injury II: Pathophysiology
Rheumatic Heart Disease I: Introduction
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Heart Failure Drugs: Diuretics
