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Probucol inhibited Nox2 expression and attenuated podocyte injury in type 2 diabetic nephropathy of db/db mice
Abstract:
The present study was conducted to investigate the effects of probucol on the progression of diabetic nephropathy and the underlying mechanism in type 2 diabetic db/db mice. Eight weeks db/db mice were treated with regular diet or probucol-containing diet (1%) for 12 weeks. Non-diabetic db/m mice were used as controls. We examined body weight, blood glucose, and urinary albumin. At 20 weeks, experimental mice were sacrificed and their blood and kidneys were extracted for the analysis of blood chemistry, kidney histology, oxidative stress marker, and podocyte marker. As a result, 24 h urinary albumin excretions were reduced after probucol treatment. There were improvements of extracellular matrix accumulation and fibronectin and collagen IV deposition in glomeruli in the probucol-treated db/db mice. The reduction of nephrin and the loss of podocytes were effectively prevented by probucol in db/db mice. Furthermore, probucol significantly decreased the production of thiobarbituric acid-reactive substances (TBARS), an index of reactive oxygen species (ROS) generation and down-regulated the expression of Nox2. Taken together, our findings support that probucol may have the potential to protect against type 2 diabetic nephropathy via amelioration of podocyte injury and reduction of oxidative stress.
Insights
Probucol treatment reduced albuminuria and protected podocytes in diabetic mice. This suggests probucol may combat type 2 diabetic nephropathy by reducing oxidative stress and podocyte injury.
Area of Science:
- Nephrology
- Endocrinology
- Pharmacology
Background:
- Diabetic nephropathy is a major complication of type 2 diabetes, characterized by kidney damage.
- Oxidative stress and podocyte injury play critical roles in the progression of diabetic nephropathy.
Purpose of the Study:
- To investigate the therapeutic effects of probucol on diabetic nephropathy in a mouse model.
- To elucidate the underlying mechanisms, focusing on oxidative stress and podocyte protection.
Main Methods:
- Type 2 diabetic db/db mice and non-diabetic db/m mice were treated with a control or probucol-containing diet for 12 weeks.
- Evaluated parameters included urinary albumin excretion, kidney histology, oxidative stress markers (TBARS, Nox2), and podocyte markers (nephrin).
Main Results:
- Probucol treatment significantly reduced 24-hour urinary albumin excretion in db/db mice.
- Histological analysis revealed improvements in extracellular matrix accumulation and reduced fibronectin and collagen IV deposition.
- Probucol prevented nephrin reduction and podocyte loss, decreased thiobarbituric acid-reactive substances (TBARS), and down-regulated Nox2 expression.
Conclusions:
- Probucol demonstrates protective effects against type 2 diabetic nephropathy in db/db mice.
- The renoprotective effects are attributed to the amelioration of podocyte injury and reduction of oxidative stress.
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