title: Sodium Citrate Inhibits Endoplasmic Reticulum Stress in Rats with Adenine-Induced Chronic Renal Failure.
abstract: OBJECTIVE
  Endoplasmic reticulum stress (ERS) is an important self-protective cellular response to harmful stimuli that contribute to various diseases, including chronic renal failure (CRF). Sodium citrate plays an important role in antioxidant and cellular immunity, but whether it improves ERS in CRF is unclear.
  
  
  METHODS
  The rats were randomly divided into five groups: the control group, the sodium citrate control group, the model group, model rats with low dose sodium citrate (216 mg/kg), and model rats with a high dose of sodium citrate (746 mg/kg). The rats were euthanized at 6, 8, 12, and 16 weeks with their blood and renal tissue in detection.
  
  
  RESULTS
  The increased concentrations of blood urea nitrogen and serum creatinine in the model group were significantly decreased by sodium citrate treatment. Hematoxylin-eosin and Masson staining showed that sodium citrate treatment apparently improved renal pathological changes in CRF rats. Western blot analysis showed that sodium citrate treatment decreased the protein levels of transforming growth factor-beta 1 and collagen type IV, which were increased in model rats. Moreover, immunohistochemical staining demonstrated that sodium citrate could effectively reduce the protein expression of glucose-regulated protein 78 kDa and CCAAT/enhancer-binding protein homologous protein in the model rats, which was consistent with western blot results. Additionally, the high dose of sodium citrate had a stronger protective effect in CRF rats than the low dose of sodium citrate.
  
  
  CONCLUSIONS
  Sodium citrate has a protective effect on CRF through its effects on ERS.
authors: Department of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
authors: Yan
authors: Y
authors: Ou
authors: Wenqian
authors: W
authors: Hou
authors: Shuiqin
authors: S
authors: Li
authors: Xiaojing
authors: X
authors: Zhu
authors: Yan
authors: Y
authors: Lin
authors: Jin
authors: J
authors: Han
authors: Zhaoyang
authors: Z
authors: Duan
authors: Baosong
authors: B
authors: Gui
mesh_terms: D051702:Activating Transcription Factor 6 / Q000378:metabolism; D000225:Adenine; D000818:Animals; D001806:Blood Urea Nitrogen; D002021:Buffers; D002951:Citrates / Q000008:administration & dosage / Q000494:pharmacology*; D024141:Collagen Type IV / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D006360:Heat-Shock Proteins / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077559:Sodium Citrate; D051742:Transcription Factor CHOP / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D019892:eIF-2 Kinase / Q000378:metabolism
chemical_list: D051702:Activating Transcription Factor 6; D000225:Adenine; D002021:Buffers; D002951:Citrates; D024141:Collagen Type IV; D003404:Creatinine; D000091342:Endoplasmic Reticulum Chaperone BiP; D006360:Heat-Shock Proteins; D000077559:Sodium Citrate; D051742:Transcription Factor CHOP; D053773:Transforming Growth Factor beta1; D019892:eIF-2 Kinase; C497113:Atf6 protein, rat