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salvianolic acid b/경색증

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Comparison of cardioprotective effects of salvianolic acid B and benazepril on large myocardial infarction in rats.

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In the present study, we compared cardioprotective effects of salvianolic acid B (Sal B) and the angiotension-converting enzyme inhibitor, benazepril, in rats with large myocardial infarction (MI). The large MI was produced by coronary artery ligation for 4 weeks in rats. The rats were divided into
The aim of this study was to compare the cardioprotective effects of salvianolic acid B (Sal B) and the angiotension-converting enzyme inhibitor, benazepril, in rats with chronic myocardial infarction (MI) that resulted from a coronary artery ligation for 4 weeks. The rats were divided into four
OBJECTIVE To observe the proliferation state of transplanted cells in acute myocardial infarction (AMI) rats, and the endothelial progenitor cells (EPCs) preconditioned by salvianolic acid B in different ratios with the bone mesenchymal stem cells (BMSCs). METHODS The cultivation and purification of
OBJECTIVE The aim of this study was to investigate the cardioprotective effect of salvianolic acid B (Sal B) on acute myocardial infarction (AMI) in rats and its potential mechanisms. METHODS The AMI model was established in rats to study the effect of Sal B on AMI. Haematoxylin-eosin (HE) staining

Ginsenoside Rg1 and Rb1, in combination with salvianolic acid B, play different roles in myocardial infarction in rats.

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BACKGROUND The herb pair of Salvia miltiorrhiza and Panax notoginseng has widely been used for improving coronary and cerebral circulation in China. However, the exact contribution of the major active components of S. miltiorrhiza and P. notoginseng to cardioprotection is far from clear. In the
OBJECTIVE To study the cardioprotective effect of salvianolic acid B (Sal B) on cardiac dysfunction. We hypothesized that hyperleptinemia may correlate with abnormal expression of sarco/endoplasmic reticulum ATPase 2a (SERCA2a), phospholamban (PLB) and endothelin-reactive oxygen species (ET-ROS)

Cardioprotective effect of SMND-309, a novel derivate of salvianolic acid B on acute myocardial infarction in rats.

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(2E)-2-{6-[(E)-2-carboxyvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, a novel compound designated SMND-309, is a new derivate of salvianolic acid B. The present study was designed to investigate the cardioprotective potential of SMND-309 and to elucidate the possible mechanisms

Cardioprotection of salvianolic acid B and ginsenoside Rg1 combination on subacute myocardial infarction and the underlying mechanism.

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Following myocardial infarction (MI), a series of structural and functional changes evolves in the myocardium, collectively defined as cardiac remodeling.The aim of present study was to investigate the cardioprotection of salvianolicacid B (SalB) and

SMND-309, a novel derivate of salvianolic acid B, ameliorates cerebral infarction in rats: characterization and role.

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(2E)-2-{6-[(E)-2-carboxylvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, a novel compound designated SMND-309, is a new degradation product of salvianolic acid B. The present study was conducted to evaluate whether SMND-309 has a protective effect on permanent focal cerebral

Comparison of cardioprotective effects of salvianolic acid B and benazepril on large myocardial infarction in rats.

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Effect and mechanism of salvianolic acid B on the myocardial ischemia-reperfusion injury in rats.

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OBJECTIVE To investigate the effect of salvianolic acid B on rats with myocardial ischemia-reperfusion injury. METHODS SD rats were randomly divided into five groups (n=10 in each group): A sham operation group, B ischemic reperfusion group model group, C low dose salvianolic acid B group, D median

Cardio-protection of salvianolic acid B through inhibition of apoptosis network.

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Targeting cellular function as a system rather than on the level of the single target significantly increases therapeutic potency. In the present study, we detect the target pathway of salvianolic acid B (SalB) in vivo. Acute myocardial infarction (AMI) was induced in rats followed by the treatment
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