title: Ginsenoside Rg1 protects chronic cyclosporin a nephropathy from tubular cell apoptosis by inhibiting endoplasmic reticulum stress in rats.
abstract: BACKGROUND
  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.
  
  
  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.
authors.affiliation: Department of Nephrology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.
authors.forename: Q-F
authors.initials: QF
authors.lastname: Liu
authors.affiliation: Department of Pathology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.
authors.forename: Z-Y
authors.initials: ZY
authors.lastname: Deng
authors.affiliation: Department of Nephrology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.
authors.forename: J-M
authors.initials: JM
authors.lastname: Ye
authors.affiliation: Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China.
authors.forename: A-L
authors.initials: AL
authors.lastname: He
authors.affiliation: Centre Laboratory, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, Jiangsu, China. Electronic address: whitelss@163.com.
authors.forename: S-S
authors.initials: SS
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002491:Central Nervous System Agents / Q000627:therapeutic use*; D016572:Cyclosporine / Q000009:adverse effects*; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D036145:Ginsenosides / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D020287:In Situ Nick-End Labeling; D008297:Male; D020011:Protective Agents / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D051436:Renal Insufficiency, Chronic / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*
chemical_list: D002491:Central Nervous System Agents; D036145:Ginsenosides; D007166:Immunosuppressive Agents; D020011:Protective Agents; D016572:Cyclosporine; D053148:Caspase 3; C035054:ginsenoside Rg1