title: [Study about cardiomyocyte apoptosis in myocardial ischemic-reperfusion injury of rats and NF-κB p65, iNOS expression].
abstract: OBJECTIVE
  By observing the rats with PDTC after the intervention, myocardial ischemic reperfusion injury (MIRI) during apoptosis, NF-κB and iNOS expression. Analysis of NF-κB and iNOS expression in the rat heart ischemic-reperfusion injury, apoptosis in the process of regulation and its mechanism.
  
  
  METHODS
  Manufacture of myocardial ischemic-reperfusion model. Using transmission electron microscope methods and TUNEL method to observe the apoptosis myocardial cells and calculated the apoptotic index; by immunohistochemistry (SP method), the detection of myocardial cell NF-κB p65 expression, and the use of immunofluorescence to detect iNOS expression in myocardial cells.
  
  
  RESULTS
  IR group and PDTC +IR group, apoptosis and NF-κB and iNOS expression was significantly stronger than that of Sham group (P<0.05). PDTC +IR group, apoptosis, NF-κB and iNOS expression was significantly weaker than the IR group, the difference was significant (P<0.05).
  
  
  CONCLUSIONS
  Myocardial ischemia reperfusion injury, there is significant apoptosis. IR can induce NF-κB activation and iNOS formation. The NF-κB activation and iNOS formation, apoptosis of cardiac muscle cells are a catalyst. PDTC can effectively reduce the expression of NF-κB, to improve the oxygen scavenging cell function, decreased cell apoptosis, reduce the MIRI injury.
authors.affiliation: Department of Anatomy, Jinggangshan University, Ji'an, China.
authors.forename: Hu
authors.initials: H
authors.lastname: Yu-hui
authors.forename: Feng
authors.initials: F
authors.lastname: Yun
authors.forename: Jiang
authors.initials: J
authors.lastname: Fen
authors.forename: Liu
authors.initials: L
authors.lastname: Xing
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D005786:Gene Expression Regulation / Q000187:drug effects; D020287:In Situ Nick-End Labeling; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism*; D011392:Proline / Q000031:analogs & derivatives / Q000494:pharmacology; D011759:Pyrrolidines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D013859:Thiocarbamates / Q000494:pharmacology; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; D011759:Pyrrolidines; D013859:Thiocarbamates; D051996:Transcription Factor RelA; C066229:prolinedithiocarbamate; D011392:Proline; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II