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Fenofibrate attenuates diabetic nephropathy in experimental diabetic rat's model via suppression of augmented
Nouf Mohamed Al-Rasheed1, Nawal Mohamed Al-Rasheed1,2, Maha Abdelrahman Al-Amin1
1a Pharmacology and Toxicology Department , College of Pharmacy, King Saud University , Riyadh , KSA.
Context:
Fibrates, the ligands of peroxisome profileferator-activated receptor-α have been shown to have a renal protective action in diabetic nephropathy (DN).
Objective:
This study aimed to elucidate the effect of fenofibrate on renal transforming growth factor-β1 (TGF-β1) and Smad3 in Streptozotocin (STZ)-induced DN.
Methods:
Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (55 mg/kg). Diabetic rats were given fenofibrate (100 mg/kg, p.o.). After 12 weeks, diabetic nephropathy biomarkers were assessed. The mRNA expression of collage I and III, TGF-β1 and Smad3 and were detected by RT-PCR.
Results:
Fenofibrate reduced significantly serum creatinine, kidney/body weight ratio, serum albumin excretion Collage I & III, TGF-β1 and Smad3 mRNA expression.
Conclusions:
Our results give further insights into the mechanisms underlying the protective role of fenofibrate in DN, suggesting that interference with TGF-β1/Smad3 signaling pathway may be a useful therapeutic approach to prevent DN.
Insights
Fenofibrate demonstrates renal protective effects in diabetic nephropathy by reducing key biomarkers and inhibiting the TGF-β1/Smad3 pathway. This suggests fenofibrate as a potential therapeutic strategy for preventing diabetic kidney disease.
Area of Science:
- Pharmacology
- Nephrology
- Molecular Biology
Background:
- Fibrates, peroxisome proliferator-activated receptor-α ligands, exhibit renal protective effects in diabetic nephropathy (DN).
- Diabetic nephropathy is a significant complication of diabetes, leading to kidney damage.
Purpose of the Study:
- To investigate the impact of fenofibrate on renal transforming growth factor-β1 (TGF-β1) and Smad3 in a rat model of STZ-induced DN.
- To elucidate the molecular mechanisms underlying fenofibrate's renoprotective action in DN.
Main Methods:
- Diabetes was induced in rats using streptozotocin (STZ).
- Diabetic rats were treated with fenofibrate (100 mg/kg).
- Renal biomarkers, including serum creatinine and albumin excretion, and mRNA expression of collagen I, III, TGF-β1, and Smad3 were assessed using RT-PCR after 12 weeks.
Main Results:
- Fenofibrate significantly reduced serum creatinine and kidney/body weight ratio.
- Treatment with fenofibrate led to decreased serum albumin excretion.
- Fenofibrate administration significantly lowered the mRNA expression of collagen I, collagen III, TGF-β1, and Smad3.
Conclusions:
- Fenofibrate exhibits a protective role in diabetic nephropathy.
- The renoprotective effects of fenofibrate may be mediated through the inhibition of the TGF-β1/Smad3 signaling pathway.
- Targeting the TGF-β1/Smad3 pathway represents a potential therapeutic strategy for preventing diabetic nephropathy.
