• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.9
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• pp.1167-1173
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• 2009

An extrapolation of bioflavone through biotransformation used Phellinus banmill KCTC16882 applied to 6 different rats group were carried out. Male Sprague-Dawley rats were fed with bioflavone free (normal: NO) diet, high-fat diet (control: CO) and diets containing 0.35%, 0.7% and 3.0% isoflavone for 8 week. Hyperlipidemia was induced by adding lard 200 g and cholesterol 10 g to CO and 0.35, 0.7 and 3.0% bioflavone diet. Bioflavone diet arrested increases in body weight without affecting feed intake in the rats. BFP-3.0 treated group showed signigicant reduction in the serum level of TG, TC and LDL-cholesterol (p<0.05) compared to the CO, while HDL-cholesterol was increased (p<0.05). The atherogenic index, ALT and AST were decreased in the BFP treated groups (p<0.05). These results suggest that consumption of BFP may lead to extrapolation of an ameliortaion of metabolic syndromes as well as a reduction of cardiovascular disease and hyperlipidemia through increasing the of HDL-cholesterol, and decreasing the level of TG in serum.

• Natural Product Sciences
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• v.11 no.3
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• pp.139-144
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• 2005

Bioflavone quercetin is believed to play an important role preventing bone loss by affecting osteoclastogenesis and regulating many systemic and local factors including hormones and cytokines. This study examined how quercetin acts on tumor necrosis factor-alpha ($TNF-{\alpha}$)-mediated apoptosis in MC3T3-E1 osteoblastic cells. Apoptosis assays revealed the dose-dependent acceleration of quercetin on $TNF-{\alpha}-induced$ apoptosis in MC3T3-E1 cells, which was demonstrated by the increased number of positively stained cells in the trypan blue staining and TUNEL assay, and the migration of many cells to the $sub-G_0/G_1$ phase in flow cytometric analysis. In particular, quercetin treatment alone increased the expression of p53 and p21 proteins in the cells. Consequently, this study showed that quercetin accelerates the $TNF-{\alpha}-induced$ apoptosis in MC3T3-E1 osteoblastic cells.

• Natural Product Sciences
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• v.11 no.2
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• pp.103-108
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• 2005

Bioflavone quercetin is thought to have an important role to inhibit bone loss by affecting osteoclastogenesis and regulating a number of systemic and local factors such as hormones and cytokines. In this study, we examined how quercetin acts on cytokine production and mineralization of osteoblast in the presence of tumor necrosis factor-alpha $(TNF-{\alpha})$ which has been known to play a pivotal role in bone metabolic diseases. Quercetin inhibited $TNF-{\alpha}-induced$ secretion of $IFN-{\gamma}$ and IL-6 in differentiated MC3T3-E1 cells. As indicated by the markers that are characteristics of the osteoblast phenotype, such as alkaline phosphatase (ALP) activity and calcium deposition, quercetin treatment slightly prevented the $TNF-{\alpha}-induced$ dramatic inhibition of differentiation and mineralization of MC3T3-E1 cells. Further, quercetin inhibited the production of nitric oxide induced by $TNF-{\alpha}$ in the cells. Collectively, our findings indicate that quercetin inhibites $TNF-{\alpha}-induced$ secretion of inflammatory cytokines in differentiated MC3T3-E1 cells without any cytotoxic effects.