title: [Effects of salidroside on tubular epithelial to myofibroblast transition under cobaltous chloride induced hypoxic status].
abstract: OBJECTIVE
  To investigate the effect and possible mechanism of salidroside on the transdifferentiation of normal rat kidney tubular epithelia cells (NRK52E) under cobaltous chloride (Co) induced hypoxic status.
  
  
  METHODS
  Cultured NRK52E cells were divided into control group, Co group and Co plus salidroside treatment groups at a dosage of 10 micromol/L, 50 micromol/L, and 100 micromol/L. Hypoxia-inducible factor-1alpha (HIF-1alpha), a master regulator of oxygen homeostasis was measured as a marker of hypoxic status. Morphologic alteration of cells was observed by inverted phase contrast microscope. The expression of alpha-SMA in NRK52E cells was detected by fluorescent immunocytochemistry (FICC) and immunohistochemistry (IHC). The alpha-SMA and TGF-beta1 mRNA were assessed using reverse transcription-polymerase chain reaction (RT-PCR). The expressions of HIF-1alpha and alpha-SMA protein were detected by Western blot analyses. The enzyme-linked immunosorbent assay was performed to detect collagen I (Col-I) and fibronectin (FN) in the supernatant.
  
  
  RESULTS
  The expression of HIF-1alpha in NRK52E cells was induced by 100 micromol/L of Co in vitro. Co induced transdifferentiation of NRK52E cells, showing fibroblast-like in morphology. Salidroside partly blocked morphologic transformation of tubular epithelial cells. Salidroside decreased the expressions of alpha-SMA protein and mRNA and TGF-beta1 mRNA significantly (P < 0.05), although they were still higher than the controls (P <0 .05). Salidroside, especially in high dosage, inhibited the increase in Col-I and FN induced by Co (P < 0.05).
  
  
  CONCLUSIONS
  Hypoxia can induce tubular epithelial-myofibroblast transdifferentiation (TEMT). Salidroside improves Co-induced hypoxic status and inhibits TEMT possibly through reducing Col I and FN in NRK52E cells.
authors.affiliation: Department of Nephrology , West China Hospital , Sichuan University, Chengdu, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Xi-Sheng
authors.initials: XS
authors.lastname: Xie
authors.forename: Fei-Yan
authors.initials: FY
authors.lastname: Li
authors.forename: He-Ping
authors.initials: HP
authors.lastname: Zhang
authors.forename: Chang
authors.initials: C
authors.lastname: Liu
authors.forename: Jun-Ming
authors.initials: JM
authors.lastname: Fan
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects*; D015687:Cell Hypoxia / Q000187:drug effects; D002460:Cell Line; D003035:Cobalt / Q000009:adverse effects; D004847:Epithelial Cells / Q000737:chemistry*; D005960:Glucosides / Q000494:pharmacology*; D007684:Kidney Tubules / Q000166:cytology*; D058628:Myofibroblasts / Q000166:cytology*; D010636:Phenols / Q000494:pharmacology*; D051381:Rats; D029771:Rhodiola / Q000737:chemistry
chemical_list: D005960:Glucosides; D010636:Phenols; D003035:Cobalt; C018021:cobaltous chloride; C009172:rhodioloside