title: [The anti-apoptosis effect of intensive insulin treatment on cardiac myocytes in severe scald rats].
abstract: OBJECTIVE
  To investigate the anti-apoptosis effect of intensive insulin treatment on cardiac myocytes and its underlying mechanism in severe scald rats.
  
  
  METHODS
  Twelve SD rats were suffered from 30% TBSA full thickness scald, and they were divided into: IT group [with intravenous injection of isotonic saline including insulin (15 mU x kg(-1) x min(-1)) and 100 g/L glucose], B group [with treatment of isotonic saline (2 mL x kg(-1) x %TBSA(-1) x 8 h(-1)]. Six SD rats received sham burn as controls[sham(S)group, with treatment of fluid at physiologic dose]. + dp/ dtmax (the rate of the rise of left ventricular pressure) and -dp/ dtmax (the rate of the fall of left ventricular pressure)at 6 post burn hour (PBH)were recorded. Apoptosis were determined by TUNEL staining and DNA ladder. The phosphorylation f Akt and protein expression of Bcl-2 in cardiomyocyte were assayed by Western blotting.
  
  
  RESULTS
  The + dp/ dtmax in the S group, IT group and B group at6 PBH were respectively (5.5 +/- 0.5) x 10(3) mm Hg/s, (3.4 +/- 0.4) x 10(3 mm Hg/s and (2.5 +/- 0.5) x 10(3) mm Hg/s (1 mm Hg = 0.133 kPa), the - dp/ dtmax were respectively (4.55 +/- 0.34) x 10(3) mmHg/s, (2.94 +/- 0.22) x 10(3) mm Hg/s and (2.05 +/- 0.19) x 10(3) mmHg/s.The +/- dp/dtmax in IT group was significantly higher than those in B group( P < 0.01). The apoptosis index in B group was (13.1 +/- 3.4)%, which was obviously higher than that in IT group (6.7 +/- 1.8)% and S group (0.6 +/- 0.4)% (P < 0.01). DNA ladder showed that no DNA fragmentation in S group, but obvious DNA fragmentation forming ladder pattern in B group, and no obvious ladder pattern in IT group. The phosphorylation of Akt and level of Bcl-2 protein in B group were markedly higher than those in IT group ( P < 0.05 or P < 0.01).
  
  
  CONCLUSIONS
  Intensive insulin treatment can upregulate the activity of Akt and enhance the expression of Bcl-2, and they might constitute the mechanisms for anti-apoptosis in cardiomyocyte and protection of cardiac function.
authors.affiliation: Burn Center of PLA, Xijing Hospital, the Fourth Military Medical University, Xián 710032, PR China.
authors.forename: Gen-fa
authors.initials: GF
authors.lastname: Lv
authors.forename: Bi
authors.initials: B
authors.lastname: Chen
authors.forename: Wan-fu
authors.initials: WF
authors.lastname: Zhang
authors.forename: Mao-long
authors.initials: ML
authors.lastname: Dong
authors.forename: Xiong-xiang
authors.initials: XX
authors.lastname: Zhu
authors.forename: Da-hai
authors.initials: DH
authors.lastname: Hu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002056:Burns / Q000188:drug therapy / Q000473:pathology*; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D007328:Insulin; D019253:Proto-Oncogene Proteins c-bcl-2; D051057:Proto-Oncogene Proteins c-akt