PMID- 22633288
OWN - NLM
STAT- MEDLINE
DCOM- 20121204
LR  - 20211203
IS  - 1618-095X (Electronic)
IS  - 0944-7113 (Linking)
VI  - 19
IP  - 8-9
DP  - 2012 Jun 15
TI  - Allicin protects against myocardial apoptosis and fibrosis in 
      streptozotocin-induced diabetic rats.
PG  - 693-8
LID - 10.1016/j.phymed.2012.04.007 [doi]
AB  - To evaluate the cardioprotective effect of allicin (AL) on myocardial injury of 
      streptozotocin (STZ)-induced diabetic rats and to further explore its underlying 
      mechanisms. Hyperglycemia was induced in rats by single intraperitoneal injection 
      of STZ (40 mg/kg). Three days after STZ induction, the hyperglycemic rats (plasma 
      glucose levels >/= 16.7 mmol/l) were treated with AL by intraperitoneal injection 
      at the doses of 4 mg/kg, 8 mg/kg, and 16 mg/kg daily for 28 days. The fasting 
      blood glucose levels were measured on every 7th day during the 28 days of 
      treatment. The body weight, blood glucose, and parameter of cardiac function were 
      detected after 4 weeks to study the cardioprotective effects of AL on diabetic 
      rats in vivo. The apoptotic index of cardiomyocytes was estimated by terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. The 
      expressions of Fas, Bcl-2, CTGF, and TGF-beta(1) protein were studied by 
      immunohistochemistry. Laser scanning confocal microscopy technique was utilized 
      to observe the effects of AL on intracellular calcium concentration ([Ca(2+)](i)) 
      in rat ventricular cardiomyocytes. AL at the doses of 4 mg/kg, 8 mg/kg, and 16 
      mg/kg significantly reduced blood glucose levels in a dose-dependent manner and 
      increased body weight as well compared with the model group. Hemodynamic 
      parameters including left ventricular systolic pressure (LVSP), left ventricular 
      end-diastolic pressure (LVEDP), and maximum rate of left ventricular pressure 
      rise and fall (+dp/dtmax and -dp/dtmax) were significantly restored back to 
      normal levels in AL-treated (8 mg/kg and 16 mg/kg) rats compared with diabetic 
      model rats. AL markedly inhibited cardiomyocyte apoptosis induced by diabetic 
      cardiac injury. Further investigation revealed that this inhibitory effect on 
      cell apoptosis was mediated by increasing anti-apoptotic protein Bcl-2 and 
      decreasing pro-apoptotic protein Fas. Additional experiments demonstrated AL 
      abrogated myocardial fibrosis by blocking the expressions of CTGF and TGF-beta(1) 
      protein. AL shows protective action on myocardial injury in diabetic rats. The 
      possible mechanisms were involved in reducing blood glucose, correcting 
      hemodynamic impairment, reducing Fas expression, activating Bcl-2 expression, 
      decreasing intracellular calcium overload, inhibiting the expressions of TGF-beta(1) 
      and CTGF, and further improving cardiac function.
CI  - Copyright (c) 2012 Elsevier GmbH. All rights reserved.
FAU - Liu, Yang
AU  - Liu Y
AD  - Department of Pharmacology, Harbin Medical University, Daqing 163319, PR China.
FAU - Qi, Hanping
AU  - Qi H
FAU - Wang, Ye
AU  - Wang Y
FAU - Wu, Mingli
AU  - Wu M
FAU - Cao, Yonggang
AU  - Cao Y
FAU - Huang, Wei
AU  - Huang W
FAU - Li, Lei
AU  - Li L
FAU - Ji, Zhong
AU  - Ji Z
FAU - Sun, Hongli
AU  - Sun H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120524
PL  - Germany
TA  - Phytomedicine
JT  - Phytomedicine : international journal of phytotherapy and phytopharmacology
JID - 9438794
RN  - 0 (Blood Glucose)
RN  - 0 (CCN2 protein, rat)
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Disulfides)
RN  - 0 (Fas protein, rat)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Sulfinic Acids)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (fas Receptor)
RN  - 139568-91-5 (Connective Tissue Growth Factor)
RN  - 3C39BY17Y6 (allicin)
RN  - 5W494URQ81 (Streptozocin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Blood Glucose/metabolism
MH  - Calcium/metabolism
MH  - Cardiotonic Agents/*pharmacology
MH  - Connective Tissue Growth Factor/metabolism
MH  - Diabetes Mellitus, Experimental/drug therapy/metabolism/*physiopathology
MH  - Disulfides
MH  - Drug Evaluation, Preclinical
MH  - Heart/drug effects
MH  - Myocardium/*pathology
MH  - Myocytes, Cardiac/drug effects/metabolism/pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Streptozocin/toxicity
MH  - Sulfinic Acids/*pharmacology
MH  - Transforming Growth Factor beta/metabolism
MH  - fas Receptor/metabolism
EDAT- 2012/05/29 06:00
MHDA- 2012/12/10 06:00
CRDT- 2012/05/29 06:00
PHST- 2011/11/04 00:00 [received]
PHST- 2012/02/28 00:00 [revised]
PHST- 2012/04/18 00:00 [accepted]
PHST- 2012/05/29 06:00 [entrez]
PHST- 2012/05/29 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
AID - S0944-7113(12)00129-8 [pii]
AID - 10.1016/j.phymed.2012.04.007 [doi]
PST - ppublish
SO  - Phytomedicine. 2012 Jun 15;19(8-9):693-8. doi: 10.1016/j.phymed.2012.04.007. Epub 
      2012 May 24.