title: [Research on olaquindox induced endoplasmic reticulum stress related apoptosis on nephrotoxicity].
abstract: OBJECTIVE
  Renal tubular epithelial cell were exposed to olaquindox and detected the ROS and apoptosis related proteins, to investigate the renal tubular epithelial cell apoptosis through endoplasmic reticulum stress mediated pathway induced by olaquindox.
  
  
  METHODS
  MTT assay (1, 2, 3, 4, 5, 6, 7and 8 μmol/ml olaquindox exposure) was used to detect the effects of olaquindox on renal tubular epithelial cell proliferation to determine test concentrations. Hoechst-33258 was used to detect morphological changes on apoptotic cells in each group. Flow cytometry method was applied to detect the apoptosis rate and intracellular reactive oxygen, and western blot assay was performed to detect the levels of endoplasmic reticulum stress-related apoptosis proteins, GRP78, GRP94 and CHOP.
  
  
  RESULTS
  According to results of the MTT test, 1, 2, 3 and 4 μmol/ml olaquindox concentrations were determined for apoptosis analysis. With the increase of olaquindox concentration, apoptosis rate and levels of endoplasmic reticulum stress related apoptosis pathway protein GRP78, GRP94 and CHOP increased, levels of ROS were increased in every groups (P < 0.05) in 2 μmol/ml olaquindox groups and above. With the prolongation of olaquindox exposure, apoptosis rate and levels of endoplasmic reticulum stress related apoptosis pathway protein GRP78 and GRP94 increased in 12 and 24 h olaquindox exposure groups, whereas in groups of olaquindox exposed for 6, 12 and 24 h, levels of ROS and endoplasmic reticulum stress related apoptosis pathway protein CHOP increased (P < 0.05).
  
  
  CONCLUSIONS
  Olaquindox can induce renal tubular epithelial cells to apoptosis and cause the renal toxicity, and the endoplasmic reticulum stress-related apoptosis maybe the associated toxicity pathway.
authors.forename: Zhongsheng
authors.initials: Z
authors.lastname: Li
authors.forename: Changyan
authors.initials: C
authors.lastname: Yu
authors.forename: Xiao
authors.initials: X
authors.lastname: Chen
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
authors.forename: Peng
authors.initials: P
authors.lastname: Cao
authors.forename: Bin
authors.initials: B
authors.lastname: Li
authors.forename: Jingwei
authors.initials: J
authors.lastname: Xiao
mesh_terms: D000818:Animals; D017209:Apoptosis; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000473:pathology*; D000091342:Endoplasmic Reticulum Chaperone BiP; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D007687:Kidney Tubules, Proximal / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D008565:Membrane Proteins; D018832:Molecular Chaperones; D011506:Proteins; D011810:Quinoxalines / Q000494:pharmacology*; D013312:Stress, Physiological / Q000187:drug effects*
chemical_list: D000091342:Endoplasmic Reticulum Chaperone BiP; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D008565:Membrane Proteins; D018832:Molecular Chaperones; D011506:Proteins; D011810:Quinoxalines; C018551:glucose-regulated proteins; C013168:olaquindox