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Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction
Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction
- 中国结合医学杂志（英文版） 2017年23卷第8期 页码：589-597
- Affiliations：
1. Graduate School, Beijing University of Chinese Medicine,Beijing,China
2. Laboratory of Academician LI Lian-da, Xiyuan Hospital, China Academy of Chinese Medical Sciences,Beijing,China
3. School of Basic Medical Sciences, Hebei University,Hebei Province,Baoding,China
- Author bio：
- Funds：Supported by the Beijing Joint Project Special Funds, and Xinjiang High Technology Research and Development Program (No. 201417111)
DOI：10.1007/s11655-016-2523-0
中图分类号：纸质出版日期：2017，
网络出版日期：2016-7-13，
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Ma, Ln., Li, Ld., Li, Sc. et al. Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction., Chin. J. Integr. Med. 23, 589–597 (2017). https://doi.org/10.1007/s11655-016-2523-0
Li-na Ma, Lian-da Li, Shao-chun Li, et al. Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction[J]. Chinese Journal of Integrative Medicine, 2017,23(8):589-597.
Ma, Ln., Li, Ld., Li, Sc. et al. Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction., Chin. J. Integr. Med. 23, 589–597 (2017). https://doi.org/10.1007/s11655-016-2523-0 DOI：
Li-na Ma, Lian-da Li, Shao-chun Li, et al. Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction[J]. Chinese Journal of Integrative Medicine, 2017,23(8):589-597. DOI： 10.1007/s11655-016-2523-0.
摘要
To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI). 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. 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). Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis
further improving cardiac function.
Abstract
To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI). 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. 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). Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis
further improving cardiac function.
关键词
allicinmyocardial infarctioncardiac functionapoptosisBcl-2/Bax
Keywords
allicinmyocardial infarctioncardiac functionapoptosisBcl-2/Bax
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