title: [Effect of 2,3-butanedione monoxime on calcium paradox-induced heart injury in rats].
abstract: OBJECTIVE
  To investigate the Effect of 2,3-butanedione monoxime (BDM) on calcium paradox-induced heart injury and its underlying mechanisms.
  
  
  METHODS
  Thirty-two adult male SD rats were randomized into 4 groups, namely the control group, BDM treatment control group, calcium paradox group, and BDM treatment group. Isolated Sprague Dawley male rat hearts underwent Langendorff perfusion and the left ventricular pressure (LVP) and left ventricular end-diastolic pressure (LVEDP) were monitored. Left ventricular developed pressure (LVDP) was calculated to evaluate the myocardial performance. Lactate dehydrogenase (LDH) content in the coronary flow was determined. Triphenyltetrazolium chloride staining was used to measure the infarct size, and myocardial cell apoptosis was tested with TUNEL method. Western blotting was used to determine the expression of cleaved caspase-3 and cytochrome c.
  
  
  RESULTS
  Compared with the control group, BDM at 20 mmol/L had no effect on cardiac performance, cell death, apoptotic index or the content of LDH, cleaved caspase-3 and cytochrome c at the end of perfusion under control conditions (P>0.05). Calcium paradox treatment significantly decreased the cardiac function and the level of LVDP and induced a larger infarct size (P<0.01), an increased myocardial apoptosis index (P<0.01), and up-regulated expressions of cleaved caspase-3 and cytochrome c (P<0.01). BDM (20 mmol/L) significantly attenuated these effects induced by calcium paradox, and markedly down-regulated the levels of LVEDP and LDH (P<0.01), lowered myocardial apoptosis index, decreased the content of cleaved caspase-3 and cytochrome c (P<0.01), increased LVDP, and reduced the infarct size (P<0.01).
  
  
  CONCLUSIONS
  BDM suppresses cell apoptosis and contracture and improves heart function and cell survival in rat hearts exposed to calcium paradox, suggesting the value of BDM as an potential drug for myocardial ischemia reperfusion injur.
authors.affiliation: Institute of Basic Medical Science, Xi'an Medical University, Xi'an 710021, China.E-mail: lhkong1984@163.com.
authors.forename: Ling-Heng
authors.initials: LH
authors.lastname: Kong
authors.forename: Xiao-Ming
authors.initials: XM
authors.lastname: Gu
authors.forename: Xing-Li
authors.initials: XL
authors.lastname: Su
authors.forename: Na
authors.initials: N
authors.lastname: Sun
authors.forename: Ming
authors.initials: M
authors.lastname: Wei
authors.forename: Juan-Xia
authors.initials: JX
authors.lastname: Zhu
authors.forename: Pan
authors.initials: P
authors.lastname: Chang
authors.forename: Jing-Jun
authors.initials: JJ
authors.lastname: Zhou
mesh_terms: D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000009:adverse effects*; D053148:Caspase 3 / Q000378:metabolism; D045304:Cytochromes c / Q000378:metabolism; D003931:Diacetyl / Q000031:analogs & derivatives* / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000139:chemically induced / Q000188:drug therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016277:Ventricular Function, Left
chemical_list: C004717:diacetylmonoxime; D045304:Cytochromes c; D007770:L-Lactate Dehydrogenase; C505410:Casp3 protein, rat; D053148:Caspase 3; D003931:Diacetyl; D002118:Calcium