Q-F Liu1, Z-Y Deng2, J-M Ye1, A-L He3, S-S Li4. 1. Department of Nephrology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China. 2. Department of Pathology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China. 3. Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China. 4. Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China. Electronic address: whitelss@163.com.
Abstract
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.
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 CsAnephropathy. 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 CsAnephropathy, at least in part, through inhibition of ER stress-triggered tubular cell apoptosis.