Juglanin alleviates myocardial injury in rats with acute myocardial infarction through modulating MAPK signaling pathway
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Keywords
Juglanin, myocardial injury, acute myocardial infarction (AMI), MAPK signaling pathway
Abstract
The aim of this study was to investigate the protective role of Juglanin in rats suffering from acute myocardial infarction (AMI). Male Sprague–Dawley (SD) mice were used to construct the AMI model. Hematoxylin and Eosin staining was used to observe the morphological changes of cardiomyocytes. Changes in lactate dehydrogenase (LDH), caspase-3 and caspase-9 were measured using commercial kits. Enzyme-linked immunosorbent assay was used to measure the serum level of creatine kinase myocardial band (CK-MB), Interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), IL-10 and IL-1β. Protein expression and phosphorylation were determined by Western blotting test. The morphology of cardiomyocytes suffered great changes because of AMI, which included focal myocardial necrosis, severe inflammatory cell infiltration, and myocardial fiber dissolution, disorder, and partial rupture. The morphological changes in cardiomyocytes were significantly ameliorated through treatment with Juglanin (10 mg/kg and 30 mg/kg). Increment of serum CK-MB, LDH, IL-6, TNF-α, IL-10 and IL-1β was reduced in AMI rats treated with 10-mg/kg and 30-mg/kg Juglanin. Cell apoptosis was also inhibited by Juglanin treatment. AMI-induced phosphorylation of p38, extracellular signal-regulated kinase (p-ERK) and c-Jun N-terminal kinase (p-JNK) was suppressed through treatment with Juglanin. This study demonstrated that Juglanin alleviated myocardial injury in rats because of AMI through inactivation of mitogen-activated protein kinase signaling pathway, thus indicating a protective role in rat AMI model.
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