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Puerarin reduces increased c-fos, c-jun, and type IV collagen expression caused by high glucose in glomerular
1Department of Pharmacology, Suzhou Institute of Chinese Materia Medica,Medical College of Soochow University, Suzhou 215007, China.
Aim:
Increased expression of c-fos, c-jun and type IV collagen (CoIV) in glomerular mesangial cells (GMC) are important characteristics of diabetic nephropathy. Both c-fos and c-jun regulate the gene expression of extracellular matrix components, and CoIV is the main component of the extracellular matrix. It has been reported that puerarin inhibits aggregation of the extracellular matrix in diabetic rats by an as yet unknown mechanism. The aim of this study is to investigate the effect of puerarin on c-fos, c-jun and CoIV expression in GMC cultured in medium containing 5.6 or 27.8 mmol/L glucose.
Methods:
The expressions of c-fos and c-jun were measured at the protein level using flow cytometry. CoIV content was detected using radioimmunoassay. Protein kinase C (PKC) activity was measured using liquid scintillation counting.
Results:
Puerarin (10(-5) mmol/L) significantly ameliorated the high-glucose effect on c-fos, c-jun and CoIV expression. This effect is accompanied by a reduced PKC activity in these cells.
Conclusion:
Our results suggest that reduced PKC activity and expression of c-fos and c-jun in GMC might participate in the mechanisms underlying the therapeutic effect of puerarin on diabetic nephropathy.
Insights
Puerarin treatment reduced high glucose-induced increases in c-fos, c-jun, and type IV collagen in kidney cells. This therapeutic effect in diabetic nephropathy may involve decreased protein kinase C activity.
Area of Science:
- Nephrology
- Endocrinology
- Molecular Biology
Background:
- Diabetic nephropathy is characterized by increased expression of c-fos, c-jun, and type IV collagen (CoIV) in glomerular mesangial cells (GMC).
- c-fos and c-jun regulate extracellular matrix gene expression, with CoIV being a primary component.
- Puerarin has shown potential in inhibiting extracellular matrix aggregation in diabetic rats via an unclear mechanism.
Purpose of the Study:
- To investigate the effects of puerarin on c-fos, c-jun, and CoIV expression in GMC.
- To explore the role of protein kinase C (PKC) activity in puerarin's mechanism of action.
Main Methods:
- Quantification of c-fos and c-jun protein levels using flow cytometry.
- Measurement of CoIV content via radioimmunoassay.
- Assessment of PKC activity using liquid scintillation counting.
Main Results:
- Puerarin (10^-5 mmol/L) significantly counteracted high glucose-induced increases in c-fos, c-jun, and CoIV expression in GMC.
- The ameliorating effect of puerarin was associated with a reduction in cellular PKC activity.
Conclusions:
- Reduced PKC activity and decreased expression of c-fos and c-jun in GMC appear to be involved in puerarin's therapeutic effects.
- These findings suggest a potential mechanism for puerarin in managing diabetic nephropathy.
