Introduction
This study tested the effect of ginsenoside Rg1 (G-Rg1) in cyclosporin A (CsA)-induced endoplasmic reticulum (ER) stress on renal tubular cell apoptosis in a rat model of chronic CsA nephropathy.
Materials and Methods
Twenty-two Sprague-Dawley rats were randomized into 3 groups: a control group, a model group (CsA 25 mg/kg per day), and a G-Rg1 treatment group (CsA 25 mg/kg per day and G-Rg1 20 mg/kg per day). We examined the effects of G-Rg1 on histopathology, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, and expression of glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein, and caspase-3 by using Western blot analysis.
Results
G-Rg1 ... More
Introduction
This study tested the effect of ginsenoside Rg1 (G-Rg1) in cyclosporin A (CsA)-induced endoplasmic reticulum (ER) stress on renal tubular cell apoptosis in a rat model of chronic CsA nephropathy.
Materials and Methods
Twenty-two Sprague-Dawley rats were randomized into 3 groups: a control group, a model group (CsA 25 mg/kg per day), and a G-Rg1 treatment group (CsA 25 mg/kg per day and G-Rg1 20 mg/kg per day). We examined the effects of G-Rg1 on histopathology, terminal deoxynucleotidyl transferase dUTP nick-end labeling staining, and expression of glucose-regulated protein 78, CCAAT/enhancer-binding protein homologous protein, and caspase-3 by using Western blot analysis.
Results
G-Rg1 attenuated CsA-induced tubulointerstitial fibrosis and reduced tubular epithelial cell apoptosis as assessed by terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and caspase-3 expression. Compared with the model group, it reduced the expression of glucose-regulated protein 78 and CCAAT/enhancer-binding protein homologous protein (0.12 ± 0.03 vs 0.48 ± 0.05 [P < .01]; 0.55 ± 0.11 vs 1.08 ± 0.07 [P < .05]), respectively.
Conclusions
G-Rg1 mitigates the progression of chronic CsA nephropathy, at least in part, through inhibition of ER stress-triggered tubular cell apoptosis.
