Flavonoids are widespread among food plants including vegetables and fruits and constitute an integral part of the human diet. Many investigators have attempted to elucidate a wide variety of their biological effects such as anti-oxiclative activity, anti-inflammatory and anti-tumor functions and so on. Our previous in vitro study showed that quercetin, a major flavonoid, has definite the inhibitory action of microtubule polymerization. In the present study, we investigated the effect of quercetin on cell proliferation and microtubule polymerization using rat prostate hyperplasia model. Male Wistar-Imamichi rats were divided into following experimental groups: group I (untreated controls); group 2 (castrated rats); group 3 (group2+1 mg/animal of testosterone-propionate +0.01 mg/animal of β-estradiol 2-benzoate ) group 4 (group 3 + 4% quercetin feeding for 2 weeks); group 5 (group 3 + 4% quercetin feeding for 5 weeks). Prostate weight significantly reduced in the group 2 compared with group I . In hormone - administered rats (group 3; hyperplasia model), prostate weight obviously increased than that of group I and group2. However the treatment of quercetin significantly inhibited the proliferation of glandular epithelial cells (group 4 and 5). Furthermore, the disassembly of microtubules was occurred in group5. It has been reported that microtubule dysfunction initiate apoptosis through the alteration of intracellular signal transduction such as c-Jun N-terminal Kinase (JNK) pathway. These results suggested that quercetin inhibits cell proliferation with microtubule dysfunction.