During inflammation, circulating conjugates of quercetin pass through the endothelium to reach vascular smooth muscle cells where they exert their biological effects and are then deconjugated (Mochizuki et al 2004).

The cardioprotective effects of quercetin may be related to its vasorelaxant (Ke Chen & Pace-Asciak 1996, Roghani et al 2004), anti-inflammatory and antioxidant properties and inhibition of vascular smooth muscle cell proliferation and migration Quercetin 976

(Alcocer et al 2002, Moon et al 2003) as demonstrated in animal and in vitro models.

Animal experiments indicate that doses of quercetin equivalent to 1-2 glasses of red wine exerts a cardioprotective effect following ischaemia-reperfusion by improving the function of mitochondria, which play a critical role in myocardial recovery (Brookes et al 2002) and may also prevent the development of atherosclerosis through several indirect mechanisms (Auger et al 2005). In humans quercetin inhibits platelet aggregation and signalling and thrombus formation at doses of 1 50 mg or 300 mg quercetin-4'-0-beta-D-glucoside (Hubbard etal 2004). This effect, however, may not occur with clinically relevant doses.

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