Guang-ming Zhang1 ,
Zhi-ying Zhao2,
Hai-juan Hu1,
Jing Yang1,
Guoqiang Gu1
1Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000;
2Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, PR China.
For correspondence:- Guang-ming Zhang
Email: guangmzhang@163.com
Accepted: 23 February 2018
Published: 31 March 2018
Citation:
Zhang G, Zhao Z, Hu H, Yang J, Gu G.
Effect of pinocembrin pre-treatment on expressions of Cx43 protein and claudin 1 in myocardial ischemia cardiomyocytes of arrhythmic rats. Trop J Pharm Res 2018; 17(3):415-422
doi:
10.4314/tjpr.v17i3.5
© 2018 The authors.
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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 up-regulation 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, Cardiomy