Abstract

BackgroundThis study aimed to investigate the effect of the Phellinus linteus (Mesima) decoction on podocyte injury in a rat model of focal and segmental glomerulosclerosis (FSGS) and evaluate the potential mechanisms.MethodsFSGS resembling primary FSGS in humans was established in rats by uninephrectomy and the repeated injection of doxorubicin. The FSGS rats were randomly divided into the model group, low-dose group of P. linteus decoction (PLD-LD), medium-dose group of P. linteus decoction (PLD-MD), and high-dose group of P. linteus decoction (PLD-HD). Blood and urine analysis were performed after 12 weeks and the molecular indicators of renal function and the renal pathological changes were examined.ResultsFSGS developed within 12 weeks in the test group and showed progressive proteinuria and segmental glomerular scarring. Urinary protein, serum creatinine, urea nitrogen, triglycerides and cholesterol were significantly reduced following the 12-week intervention with P.linteus decoction, especially in the PLD-LD group. Renal nephrin and podocin were markedly increased. Moreover, the pathological damage in the renal tissue was alleviated by the PLD-LD intervention.ConclusionThe P. linteus decoction alleviated the podocyte injury in the FSGS rat model, thus minimizing the progression of glomerular sclerosis and improving renal function.

Highlights

  • This study aimed to investigate the effect of the Phellinus linteus (Mesima) decoction on podocyte injury in a rat model of focal and segmental glomerulosclerosis (FSGS) and evaluate the potential mechanisms

  • Effect of P. linteus decoction on urinary protein excretion in FSGS rats To establish a model for rat FSGS, we subjected rats to uninephrectomy followed by repeated injection of doxorubicin

  • These results indicate that the PLD-LD can attenuate urinary protein excretion and improve the serum ALB levels in the FSGS rat

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Summary

Introduction

This study aimed to investigate the effect of the Phellinus linteus (Mesima) decoction on podocyte injury in a rat model of focal and segmental glomerulosclerosis (FSGS) and evaluate the potential mechanisms. Focal and segmental glomerulosclerosis (FSGS) represents a frequently occuring glomerular kidney disease [1]. It is usually delineated as a clinical-pathologic syndrome manifesting proteinuria, and focal and segmental glomerular sclerosis with foot process effacement [2]. The main clinical manifestation of FSGS is proteinuria. The first-line of treatment in idiopathic FSGS with nephritic syndrome is a prolonged course of corticosteroids [3]. The occurrence of steroid resistance or steroid dependence is commonly reported. FSGS may still result in end-stage renal failure despite

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