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Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary
BROMELAIN INDUCES CARDIOPROTECTION AGAINST ISCHEMIA-REPERFUSION INJURY THROUGH AKT/FOXO PATHWAY IN RAT MYOCARDIUM
Abstract number: P32
Juhasz1 B., Varga1 B., Gesztelyi1 R., Wachal1 Z., Maulik2 N., Tosaki1 Á.
Aims:
Bromelain (Br), a proteolytic enzyme extracted from the stem of the pineapple, is known to possess anti-inflammatory activity and has been shown to reduce blood viscosity, prevent the aggregation of blood platelets, and improve ischemia-reperfusion (I/R) injury in a skeletal muscle model.
Methods:
We investigated the capacity of Br to limit myocardial injury in a global I/R model. Adult male Sprague-Dawley rats were divided into two groups: control (PBS) and Br at 10 mg/kg in PBS administered via intraperitoneal injection (twice/day) for 15 consecutive days. On day 16, the hearts were excised and subjected to 30 min of global ischemia followed by 2 h of reperfusion.
Results:
Bromelain-treated rats showed higher left ventricular functional recovery throughout reperfusion compared with the controls [maximum rate of rise in intraventricular pressure (dP/dt max), 2,225 vs. 1,578 mmHg/s at 2 h reperfusion]. Aortic flow was also found to be increased in Br treatment when compared with that in untreated rats (11 vs. 1 ml). Furthermore, Br treatment reduced both the infarct size (34% vs. 43%) and the degree of apoptosis (28% vs. 37%) compared with the control animals. Western blot analysis showed an increased phosphorylation of both Akt and FOXO3A in the treatment group compared with the control.
Conclusion:
These results demonstrated for the first time that bromelain triggers an Akt-dependent survival pathway in the heart, revealing a novel mechanism of cardioprotective action and a potential therapeutic target against I/R injury.
Support:
National Heart, Lung, and Blood Institute Grants HL-56803, HL-69910, and HL-85804 and National Institutes of Health Grant NCCAM5F32-AT001569, OTKA 78223
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :P32