P628Increased myocardial connexin-43 and PKC-epsilon signaling is most likely implicated in cardioprotective effects of red palm oil demonstrated in SHR

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Background and Purpose

We have previously shown cardiac benefit of omega-3 unsaturated fatty acids supplementation of SHR due to up-regulation of myocardial cell-to-cell channel protein, connexin43 (Cx43). Recently, the cardio-protective effect of red palm oil (RPO) containing 50% saturated fatty acids, carotenoids, tocoferol and tocotrienols has been reported. The purpose of this study was to examine whether RPO supplementation may affect myocardial Cx43 and PKC-epsilon signaling and consequently both propensity of hypertensive rat heart to arrhythmias and heart function.

Design and Methods

Male SHR and normotensive WKY rats were fed a standard rat chow plus RPO (200microL/day) for 5 weeks and were compared with untreated rats. Ventricular tissue was used for real time PCR, immunoblotting and immunostaining to determine Cx43 mRNA, its protein levels and in situ distribution as well as for PKC-epsilon expression. Langendorff-perfused rat heart was used to examine of post-ischemic reperfusion-induced arrhythmias, electrically inducible ventricular fibrillation and heart function.

Key results

Compared to untreated rats myocardial Cx43-mRNA levels were increased in RPO supplemented SHR. Total levels of Cx43 and its functional phosphorylated forms were reduced in untreated SHR, but increased due to the treatment, which in addition attenuated altered myocardial Cx43 distribution. Furthermore, RPO enhanced PKC-epsilon expression. These effects were associated with suppression of reperfusion-related ventricular tachycardia and electrically-inducible ventricular fibrillation. Moreover, RPO treatment of SHR resulted in an increase of coronary flow and the indexes of contraction and relaxation during post-ischemic reperfusion. However, treatment dose of RPO caused down-regulation of myocardial Cx43 and did not affect PKC-epsilon expression in WKY rats. It was associated with poor arrhythmia protection and depression of heart function.


Results indicate that SHR benefit from RPO supplementation due its apparent anti-arrhythmic and post-ischemic reperfusion-related cardioprotective effects. This protection can be, in part, linked to up-regulation of myocardial Cx43 and PKC-epsilon. Further studies should elucidate whether it might be attributed mainly to RPO-related antioxidant effects.


This work was supported by VEGA 2/0046/12 grant.

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