title: Tribulosin protects rat hearts from ischemia/reperfusion injury.
abstract: OBJECTIVE
  To investigate the protective effect of tribulosin, a monomer of the gross saponins from Tribulus terrestris, against cardiac ischemia/reperfusion injury and the underlying mechanism in rats.
  
  
  METHODS
  Isolated rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion using Langendorff's technique. The hearts were assigned to seven groups: control, ischemia/reperfusion (I/R), treatment with gross saponins from Tribulus terrestris (GSTT) 100 mg/L, treatment with tribulosin (100, 10, and 1 nmol/L) and treatment with a PKC inhibitor (chelerythrine) (1 micromol/L). Infarct size was assessed by triphenyltetrazolium chloride staining. Malondialdehyde (MDA), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) contents as well as superoxide dismutase (SOD) and creatine kinase (CK) activities were determined after the treatment. Histopathological changes in the myocardium were observed using hematoxylin-eosin (H&E) staining. Apoptosis was detected with terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. Bcl-2, Bax, caspase-3, and PKCepsilon protein expression were examined using Western blotting.
  
  
  RESULTS
  Tribulosin treatment significantly reduced MDA, AST, CK and LDH contents, and increased the activity of SOD. The infarct size of I/R group was 40.21% of the total area. GSTT and various concentrations of tribulosin treatment decreased the infarct size to 24.33%, 20.24%, 23.19%, and 30.32% (P<0.01). Tribulosin treatment reduced the myocardial apoptosis rate in a concentration-dependent manner. Bcl-2 and PKCepsilon protein expression was increased after tribulosin preconditioning, whereas Bax and caspase-3 expression was decreased. In the chelerythrine group, Bcl-2 and PKCepsilon expression was decreased, whereas Bax and caspase-3 expression was increased.
  
  
  CONCLUSIONS
  Tribulosin protects myocardium against ischemia/reperfusion injury through PKCepsilon activation.
authors.affiliation: Department of Pharmacology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Zhang
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.forename: Shi-jie
authors.initials: SJ
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D053148:Caspase 3 / Q000378:metabolism; D004789:Enzyme Activation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D008517:Phytotherapy; D051744:Protein Kinase C-epsilon / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012855:Sitosterols / Q000627:therapeutic use*; D032444:Tribulus; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D002316:Cardiotonic Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D012855:Sitosterols; D051028:bcl-2-Associated X Protein; C472188:tribulosin; D051744:Protein Kinase C-epsilon; D053148:Caspase 3
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