Journal
INFLAMMATION
Volume 41, Issue 2, Pages 432-436Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-017-0699-x
Keywords
morroniside; acute myocardial infarction (AMI); cardioprotection
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Funding
- National Science and Technology Major Project [2012ZX09102201-106]
- National Natural Science Foundation of China [81373994, 81573633, 81503049, 81173575]
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The aim of this study is to investigate the cardioprotective effects of morroniside in rats following acute myocardial infarction. An acute myocardial infarction (AMI) was induced by ligating the anterior descending coronary artery (LAD) [1]. Following AMI, morroniside was administered intragastrically for 24 h at doses of 45, 90, and 180 mg/kg, respectively. Biomarkers such as creatine kinase (CK-MB), lactate dehydrogenase (LDH), E-hydroxybutyrate dehydrogenase (E-HBDH), and aspartate aminotransferase (AST) activities in AMI rats in the serum were detected with commercial kits [2]. Following AMI, morroniside was administered intragastrically for 72 h at doses of 45, 90, and 180 mg/kg/d, respectively. The expression of nuclear factor kappa B (NF-kappa B) in cardiac myocardium was detected by western blotting analysis. Meanwhile, cardiac function was measured by echocardiography. We observed morroniside decreased the levels of CK-MB, LDH, E-HBDH, and AST activities in AMI rats after 24 h. We also found that morroniside reduced the expression of NF-kappa B in cardiac myocardium at 72 h post AMI rats. Further, cardiac function was improved by administration of morroniside. Collectively, our findings demonstrated that morroniside had cardioprotective effects in rats following acute myocardial infarction. Attenuation of inflammation might contribute to the cardioprotective effects of morroniside.
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