title: Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction.
abstract: OBJECTIVE
  To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI).
  
  
  METHODS
  Ninety-four Wistar rats were randomly assigned to 6 groups (n=14-16 per group): sham control group [underwent thoracotomy without left anterior descending (LAD) occlusion and only received an injection of the same amount of citrate buffer], MI control group (subjected to LAD occlusion and only received an injection of same amount of citrate buffer), positive control group (subjected to LAD occlusion and received an injection of diltiazem hydrochloride at the dose of 1.5 mg/kg), and MI + allicin groups (subjected to LAD occlusion and received an injection of allicin at the doses of 1.2, 1.8, and 3.6 mg/kg). All of the drugs were administered intraperitoneally daily for 21 days. The infarct area was measured by myocardial staining. Hematoxylin-eosin staining was used to observe the pathological changes. Cardiac function parameters were assessed by echocardiography. The myocardial apoptotic index was estimated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. The expression of Bax and Bcl-2 were detected by quantificational real-time polymerase chain reaction and Western blot.
  
  
  RESULTS
  Treatment with allicin could attenuate the myocardial infarct area (P<0.05) and relieve the changes of the myocardium. The left ventricular anterior wall diastolic and systolic thicknesses were increased in the allicin-treated groups (P<0.05), while there was no signifificant difference in the left ventricular posterior wall diastolic and systolic thickness (P>0.05). The left ventricular internal diameter in systole, ejection fraction, fractional shortening, and stroke volume were dramatically elevated in allicin-treated rats (P<0.05). Allicin dose-dependently reduced creatine kinase and lactate dehydrogenase levels (P<0.05). The myocardial apoptotic index was also markedly lowered, and Bax expression was signifificantly decreased, whereas Bcl-2 expression exhibited an opposite trend in allicin-treated rats (P<0.05).
  
  
  CONCLUSIONS
  Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function.
authors.affiliation: Graduate School, Beijing University of Chinese Medicine, Beijing, 100029, China.|Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Ma
authors.affiliation: Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China. lilianda1934@163.com.
authors.forename: Lian-da
authors.initials: LD
authors.lastname: Li
authors.affiliation: Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.|School of Basic Medical Sciences, Hebei University, Baoding, Hebei Province, 071000, China.
authors.forename: Shao-Chun
authors.initials: SC
authors.lastname: Li
authors.affiliation: Graduate School, Beijing University of Chinese Medicine, Beijing, 100029, China.|Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
authors.forename: Xin-Mei
authors.initials: XM
authors.lastname: Hao
authors.affiliation: Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
authors.forename: Jin-Yan
authors.initials: JY
authors.lastname: Zhang
authors.affiliation: Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
authors.forename: Ping
authors.initials: P
authors.lastname: He
authors.affiliation: Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
authors.forename: Yi-Kui
authors.initials: YK
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D004220:Disulfides; D015536:Down-Regulation / Q000187:drug effects; D006334:Heart Function Tests / Q000187:drug effects*; D020287:In Situ Nick-End Labeling; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D017208:Rats, Wistar; D013441:Sulfinic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D004220:Disulfides; D013441:Sulfinic Acids; D051028:bcl-2-Associated X Protein; C006452:allicin; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase
keywords: Bcl-2/Bax; allicin; apoptosis; cardiac function; myocardial infarction