Natural honey: a new and potent anti-angiogenic agent in the air-pouch model of inflammation.

Despite reports indicating anti-inflammatory effects of honey, the anti-angiogenic effect of honey and its impact on inflammatory mediators in the air pouch model of inflammation have not yet been studied. The aims of present study were to investigate the effects of honey on angiogenesis, inflammatory cytokine vascular endothelial growth factor (VEGF) level as an important marker of angiogenesis and prostaglandin E2 (PGE2) in the rat air pouch model of inflammation. Male Wistar rats were anesthetized, and then 20 ml and 10 ml of sterile air were injected subcutaneously in the back on days 0 and 3, respectively. On day 6, inflammation was induced by injection of 1 ml of carrageenan 1% into pouches. After 72 h, the rats were sacrificed; pouch fluid was collected in order to determine PGE2 concentration and VEGF level. The Pouches were dissected out and weighed. Angiogenesis of granulomatous tissue was assayed using a hemoglobin kit. Honey was able to reduce granulation tissue weight and angiogenesis as well as showing potent inhibitory activities against PGE2 and VEGF in air pouch model of inflammation. The decrease in angiogenesis correlates with the inhibition of PGE2 and VEGF. Honey is potentially useful in the treatment of granulomatous inflammatory conditions. It seems that the anti-angiogenic activities of honey are mediated through modulation of PGE2 and VEGF production.

Antiarrhythmic and arrhythmogenic effects of L-carnitine in ischemia and reperfusion.

Isolated rat hearts were subjected to 30-min coronary artery occlusion followed by 120-min reperfusion. The hearts (n=8-12) were perfused with Krebs-Henseleit solution enriched with L-carnitine (0.5, 2.5 and 5 mM) for 10 min before and after ischemia or reperfusion and for the whole period of ischemia and reperfusion. Two-hour perfusion with L-carnitine during ischemia/reperfusion markedly (p<0.05) and dose-dependently decreased the incidence of ventricular tachycardia (VT, maximum 65%). The incidence of reperfusion ventricular fibrillation (VF) also decreased from 63% (control) to 17% in hearts perfused with 5 mM L-carnitine, as reflected by a significant (p<0.05) decline in VF duration from 218+/-99 sec in control to 19+/-19 sec. Perfusion of etomoxir (palmitoylcarnitinetransferase-1 inhibitor) along with L-carnitine reversed the antiarrhythmogenic action of L-carnitine. Interestingly, short time preischemic administration of L-carnitine produced a concentration-dependent arrhythmogenic effects on both ischemia and reperfusion-induced arrhythmias. These results show that L-carnitine produced a protective effect against reperfusion arrhythmias only when it was perfused for the whole period of the experiment. This protective action was reversed by concomitant use of etomoxir, suggesting that the efficacy of L-carnitine is due to its mitochondrial action but cannot be solely attributed to increased fatty acid oxidation.