title: [Voltage dependent anion channel 2 involved mitochondrial apoptosis and its possible regulatory signal pathway in hearts of rats with severe scalds].
abstract: OBJECTIVE
  To explore the role of voltage dependent anion channel 2 (VDAC2) involved mitochondrial apoptosis in heart injury of rats with severe scald injury and elucidate its possible regulatory signal pathway.
  
  
  METHODS
  A total of 60 Wistar rats were divided into sham scald group (n = 30) and scald group (n = 30) according to a random digital table. Blood and heart tissue samples were harvested at Day 1, 7, 14 post scalding. Myocardial injury was assessed with cardiac troponin I (cTnI) by enzyme-linked immunosorbent assay (ELISA). Mitochondrial apoptosis activation was evaluated by the expressions of Bax/Bcl-2 ratio, cytoplasmic cytochrome C and VDAC2. And the levels of phosphatidylinositol 3-kinase, p-Glycogen Synthase Kinase-3β and hexokinase 2 protein were determined by Western blot.
  
  
  RESULTS
  The serum levels of cTnI were significantly higher in scald group than those in sham scald group at Day 1, 7, 14 ((1.41 ± 0.25) vs (0.53 ± 0.23) µg/L, (1.93 ± 0.53) vs (0.43 ± 0.23) µg/L, (1.62 ± 0.34) vs (0.41 ± 0.22) µg/L respectively, all P < 0.05). Compared with sham scald group, Bax/Bcl-2 ratio increased significantly in scald group at Day 1, 7 day post-scalding (3.360 ± 0.173 vs 0.623 ± 0.044, 2.736 ± 0.341 vs 0.698 ± 0.064, 1.290 ± 0.234 vs 0.718 ± 0.063 respectively, all P < 0.05), VDAC2 protein level in scald group decreased significantly at Day 1, 7, 14 (0.070 ± 0.009 vs 0.328 ± 0.026, 0.007 ± 0.002 vs 0.291 ± 0.025, 0.009 ± 0.004 vs 0.302 ± 0.037 respectively, all P < 0.05), the cytoplasmic levels of cytochrome increased significantly in scald group at Day 1, 7, 14 (0.418 ± 0.030 vs 0.022 ± 0.007, 1.685 ± 0.169 vs 0.030 ± 0.011, 0.300 ± 0.037 vs 0.098 ± 0.014 respectively, all P < 0.05), the expression of PI3K was significantly lower in scald group at Day 14 post-scalding (0.083 ± 0.015 vs 0.328 ± 0.011, P < 0.05), the expressions of p-GSK3β all reduced significantly at Day 1, 7, 14 (0.098 ± 0.014 vs 0.446 ± 0.031, 0.064 ± 0.002 vs 0.476 ± 0.054, 0.074 ± 0.010 vs 0.442 ± 0.041, respectively, all P < 0.05) and the expressions of HK2 were lower at Day 7, 14 post-scalding (0.390 ± 0.027 vs 0.611 ± 0.070, 0.267 ± 0.018 vs 0.490 ± 0.042, respectively, all P < 0.05).
  
  
  CONCLUSIONS
  VDAC2 involved mitochondrial apoptosis is activated in myocardium after severe scalds. And it may be regulated by the pathway of PI3K-GSK-HK2.
authors.affiliation: Department of Burns and Plastic Surgery, General Hospital of PLA, Beijing, China.
authors.forename: Yong-qiang
authors.initials: YQ
authors.lastname: Feng
authors.forename: Jia-ke
authors.initials: JK
authors.lastname: Chai
authors.forename: Wan-li
authors.initials: WL
authors.lastname: Chu
authors.forename: Hong-jie
authors.initials: HJ
authors.lastname: Duan
authors.forename: Li
authors.initials: L
authors.lastname: Ma
authors.forename: Hai-jun
authors.initials: HJ
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002056:Burns / Q000378:metabolism* / Q000473:pathology; D004195:Disease Models, Animal; D008928:Mitochondria / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D050996:Voltage-Dependent Anion Channel 2 / Q000378:metabolism*
chemical_list: C494767:Vdac2 protein, rat; D050996:Voltage-Dependent Anion Channel 2