[The effects of blocking intrarenal renin-angiotensin system on the expression of transforming growth factor-beta1 mRNA and extracellular matrix components]
Related Experiment Video
Updated: Oct 2, 2026

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
Published on: October 26, 2020
1Department of Nephrology, First Hospital, Beijing Medical University, Beijing 100034.
Objective:
To explore the possible mechanism of benazepril in diminishing the progression of the renal diseases.
Methods:
Experimental glomerulosclerosis in rats was induced by adriamycin. The treated group was given benazepril (4 mg x kg(-1) x d(-1)). Intrarenal angiotensin converting enzyme (ACE) activity and angiotensin II (AngII) concentration were measured with colorimetry and radioimmunoassay respectively. Immunohistochemistry staining was employed for transforming growth factor beta1 (TGF beta1) and extracellular matrix (ECM) examination. To observe the expression of TGFbeta1 mRNA in the kidney, in situ hybridization was performed.
Results:
In the rats treated with benazeapril, ACE activity and Ang II concentration in renal tissue were significantly inhibited. In the meantime, expression of TGFbeta1 mRNA and TGFbeta1 protein were down-regulated, accompanied by decreasing accumulation of ECM (compared with the untreated rats, P < 0.01).
Conclusion:
Benazepril plays an important role in down-regulating the expression of TGFbeta1 and decreasing the accumulation of ECM by blocking intrarenal renin-angiotensin system.
Insights
Benazepril inhibits renal angiotensin converting enzyme (ACE) activity, reducing angiotensin II (AngII) levels. This mechanism diminishes transforming growth factor beta1 (TGF-β1) expression and extracellular matrix accumulation, slowing kidney disease progression.
Area of Science:
- Nephrology
- Pharmacology
- Molecular Biology
Context:
- Diabetic nephropathy and glomerulosclerosis are significant causes of chronic kidney disease.
- The intrarenal renin-angiotensin system plays a crucial role in the pathogenesis of renal fibrosis.
- Identifying therapeutic targets to inhibit renal disease progression is a key research area.
Purpose:
- To investigate the mechanism by which benazepril ameliorates kidney disease progression.
- To evaluate the effect of benazepril on intrarenal angiotensin converting enzyme (ACE) activity and angiotensin II (AngII) levels.
- To assess the impact of benazepril on transforming growth factor beta1 (TGF-β1) and extracellular matrix (ECM) deposition in a rat model of glomerulosclerosis.
Summary:
- Adriamycin-induced glomerulosclerosis in rats was treated with benazepril.
- Benazepril significantly inhibited intrarenal ACE activity and AngII concentration.
- This was associated with down-regulated TGF-β1 mRNA and protein expression, and reduced ECM accumulation (P < 0.01).
Impact:
- Benazepril effectively blocks the intrarenal renin-angiotensin system.
- This action leads to decreased TGF-β1 expression and reduced ECM accumulation.
- These findings highlight benazepril's potential as a therapeutic agent for slowing the progression of renal diseases.
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