Naringin ameliorates experimental diabetic renal fibrosis by inhibiting the ERK1/2 and JNK MAPK signaling pathways

Abstract

Aims: With the specific pharmacological activities including anti-inflammation, anti-oxidant and hypoglycemic effects, Naringin may possess the potential to ameliorate diabetic nephropathy (DN). The purpose of this study was to investigate the anti-DN effect of Naringin and the molecular mechanism by which Naringin ameliorates diabetic renal fibrosis. Methods: The effects of Naringin on fibronectin (FN) and intercellular adhesion molecule (ICAM-1) as well as the MAPK signaling pathways were detected in streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-cultured glomerular mesangial cells (GMCs) respectively. Results: Naringin significantly alleviated the renal fibrosis injury and suppressed the expression of FN and ICAM-1, with down-regulating the phosphorylation of ERK1/2 and JNK and inhibiting the activation of the downstream activating protein (AP-1). There were no meaningful difference between Naringin and the MAPK specific inhibitors. Conclusion: Inhibiting the ERK1/2 and JNK MAPK signaling pathways is probably a novel mechanism by which Naringin alleviates experimental diabetic renal fibrosis.

Keywords

• Naringin
• Diabetic renal fibrosis
• Fibronectin
• Intercellular adhesion molecule
• MAPK signaling pathway