title: [Effects of propofol on PI3K/Akt signaling pathway and endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts].
abstract: OBJECTIVE
  To explore the effects of propofol on the PI3K/Akt signaling pathway and the endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts.
  
  
  METHODS
  Forty isolated rat hearts were completely randomly assigned into 5 different groups: control (C), ischemia/reperfusion (I/R), propofol (P), propofol plus Wortmannin (P + Wort) and Wortmannin (W). The isolated hearts were perfused on a Langendorff apparatus. Except for group C, all hearts were subjected to 30 min global ischemia and 120 min reperfusion. In the P, P + W and W groups, 50 µmol/L propofol or 50 µmol/L propofol + 100 nmol/L Wortmannin or 100 nmol/L Wortmannin were respectively added in the K-H buffer to perfuse for 10 min at pre-ischemia and 20 min at the beginning of reperfusion. The parameters of cardiac function were recorded at pre-ischemia and at the 120 min of reperfusion. The apoptotic index was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (Tunel). The expressions of caspase-12 and CCAAT/C/EBP homologous protein (chop) were measured by immunohistochemistry while those of Akt and p-Akt (Ser473) detected by Western blot.
  
  
  RESULTS
  Compared with the I/R group, LVEDP significantly deceased and +dp/dtmax significantly increased, the apoptotic index [(27.89 ± 1.04)% vs (33.70 ± 2.20)%], the expressions of caspase-12 [(0.1728 ± 0.0096) vs (0.2332 ± 0.0114)] and chop [(0.1889 ± 0.0078) vs (0.2407 ± 0.0123)] significantly deceased while that of p-Akt (Ser473) significantly increased in Group P (P < 0.05). Wortmannin abolished the partial protective effects of propofol postconditioning (P < 0.05).
  
  
  CONCLUSIONS
  Propofol perfusion may attenuate the endoplasmic reticulum stress pathway of apoptosis induced by ischemia/reperfusion in isolated rat hearts partly through the PI3K/Akt signal pathway.
authors.affiliation: Department of Anesthesiology, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
authors.forename: Liu
authors.initials: L
authors.lastname: Liu
authors.forename: Yong
authors.initials: Y
authors.lastname: Pang
authors.forename: Dong-wei
authors.initials: DW
authors.lastname: He
authors.forename: Xin-wei
authors.initials: XW
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D006321:Heart / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D015742:Propofol / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D015742:Propofol