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Published:
May 9, 2018DOI:
10.4314/tjpr.v17i3.5Keywords:
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Main Article Content
Effect of pinocembrin pre-treatment on expressions of Cx43 protein and claudin 1 in myocardial ischemia cardiomyocytes of arrhythmic rats
Abstract
Purpose: To investigate the effects of pinocembrin on ventricular rhythm and the expression of cardiomyocyte ligament junction protein (Cx43) and claudin 1 (ZO-1) in ischemia/reperfusion (I/R) rats.
Methods: Ischemia/reperfusion (I/R) model rats (n = 15) were divided into 5 groups: IR group, control group, and 3 pinocembrin groups (3, 10 and 30 mg/kg). The serum levels of creatine kinase-MB isoenzyme (CK-MB) and troponin I (cTnI) were measured by enzyme-linked immunosorbent assay (ELISA). Changes in myocardial tissue were detected by H & E staining, while mRNA and protein levels of Cx43, ZO-1 and Kir2.1 were measured by reverse transcriotion-polymerase chain reaction (RT-PCR) and Western blotting, respectively.
Results: In pinocembrin groups, heart rate (HR), mean arterial pressure (MAP) and rate-pressure product (RPP) levels were significantly higher compared with IR group (p < 0.05). Moreover, the extent of arrhythmia and the levels of CK-MB and cTnI in pinocembrin groups were lower relative to IR group, while Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities, as well as Cx43 mRNA, ZO-1 mRNA, and protein levels of Cx43, ZO-1 and Kir2.1 were significantly higher than the corresponding values for IR group (p < 0.05).
Conclusion: These results suggest that pinocembrin reduces ventricular arrhythmias in I/R rats by upregulation of expressions of Cx43, ZO-1 and Kir21, and inhibition of re-distribution of ZO-1 and Cx43. These findings provide the basis for the clinical application of pinocembrin in the treatment of arrhythmia.
Keywords: Pinocembrin, Ventricular arrhythmia, Ligament junction protein, Recombinant human Kir2.1 protein, Arterial pressure, Protein levels, Claudin, Cardiomyocyte
