Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats
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OriginalPaper|Updated:2021-08-27
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Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats
Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats
中国结合医学杂志(英文版)2010年16卷第2期 页码:162-166
Affiliations:
Department of Cardiac Surgery, the First Affiliated Hospital, China Medical University,Shenyang,China
Author bio:
Funds:
Supported by the Research Project of Education Department of Liaoning Province (No. 2004C050) in 2005 and Project of Technology Department of Liaoning Province (No. 2006401013-2) in 2006.
Wang, Xd., Gu, Tx., Shi, Ey. et al. Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats., Chin. J. Integr. Med. 16, 162–166 (2010). https://doi.org/10.1007/s11655-010-0162-4
Xiao-dong Wang, Tian-xiang Gu, En-yi Shi, et al. Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats[J]. Chinese Journal of Integrative Medicine, 2010,16(2):162-166.
Wang, Xd., Gu, Tx., Shi, Ey. et al. Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats., Chin. J. Integr. Med. 16, 162–166 (2010). https://doi.org/10.1007/s11655-010-0162-4DOI:
Xiao-dong Wang, Tian-xiang Gu, En-yi Shi, et al. Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats[J]. Chinese Journal of Integrative Medicine, 2010,16(2):162-166. DOI: 10.1007/s11655-010-0162-4.
Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats
摘要
To investigate the effects and mechanisms of panaxoside Rg1 on the new vessel formation in acute myocardial infarction (AMI) rats. The AMI model of male Sprague-Dawley (SD) rats was established
and rats were randomly divided into the AMI model group
the treatment group of panaxoside Rg1
the placebo group and the treatment group of panaxoside Rg1 plus rapamycin. Cardiac creatases were determined with 1 mL blood drawn from vena caudalis of the rats 48 h after the model was successfully made. After 4 weeks
Evans blue was injected into the aorta roots of the rats
and then
red tetrazoline was dyed again and the myocardial infarction area was evaluated. The microvessel density (MVD) of infarction area was determined by the immunohistochemistry of CD31; enzyme-linked immunosorbent assay (ELISA) was used to detect the protein content of CD31 and hypoxia inducible factor-1α (HIF-1α) of the infarction area. The MVD in the infarction area and the contents of CD31 and HIF-1α in the Rg1 treatment group were higher than those in the AMI model group significantly (P<0.05). The cardiac creatase and infarction area were lower in the Rg1 treatment group than those in the AMI model group significantly (P<0.05). The above effects
however
disappeared when rapamycin
the antagonist of mammalian target of rapamycin (mTOR)
was administered simultaneously. Panaxoside Rg1 could increase the expression of HIF-1α and CD31 of myocardium and stimulate the angiogenesis. The above mentioned role of panaxoside Rg1 might be related to the excitation of mTOR receptor.
Abstract
To investigate the effects and mechanisms of panaxoside Rg1 on the new vessel formation in acute myocardial infarction (AMI) rats. The AMI model of male Sprague-Dawley (SD) rats was established
and rats were randomly divided into the AMI model group
the treatment group of panaxoside Rg1
the placebo group and the treatment group of panaxoside Rg1 plus rapamycin. Cardiac creatases were determined with 1 mL blood drawn from vena caudalis of the rats 48 h after the model was successfully made. After 4 weeks
Evans blue was injected into the aorta roots of the rats
and then
red tetrazoline was dyed again and the myocardial infarction area was evaluated. The microvessel density (MVD) of infarction area was determined by the immunohistochemistry of CD31; enzyme-linked immunosorbent assay (ELISA) was used to detect the protein content of CD31 and hypoxia inducible factor-1α (HIF-1α) of the infarction area. The MVD in the infarction area and the contents of CD31 and HIF-1α in the Rg1 treatment group were higher than those in the AMI model group significantly (P<0.05). The cardiac creatase and infarction area were lower in the Rg1 treatment group than those in the AMI model group significantly (P<0.05). The above effects
however
disappeared when rapamycin
the antagonist of mammalian target of rapamycin (mTOR)
was administered simultaneously. Panaxoside Rg1 could increase the expression of HIF-1α and CD31 of myocardium and stimulate the angiogenesis. The above mentioned role of panaxoside Rg1 might be related to the excitation of mTOR receptor.
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相关机构
Department of Integrative Cardiology, China-Japan Friendship Hospital
Department of Cardiology, China-Japan Friendship Hospital
Department of Biochemistry, Institute of Basic Medicine, Shanghai University of Traditional Chinese Medicine
Department of Integrated Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Tecnology
Department of Laboratory, Ruijin Hospital Affiliated to the Medical College of Shanghai Jiao Tong University