• Journal of Nutrition and Health
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• v.40 no.8
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• pp.693-700
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• 2007

This study was performed to investigate the effects of genistein, a kind of soy isoflavones, on fatty liver and lipid metabolism in rats fed high fat diet. Twenty four male Sprague-Dawley rats were divided into four groups by dietary fat and genistein contents then raised for six weeks. The rats(n=6/group) were fed normal fat diet(NOR), high fat diet (HF), high fat with 0.1% genistein(HF+0.1%G) or high fat with 0.2% genistein(HF+0.2%G). Hepatic total lipid, triglyceride, total cholesterol and Serum GPT, as a marker for fatty liver, were significantly increased by high fat diet. Also, serum total lipid, triglyceride, total cholesterol, glucose and insulin concentration, hepatic lipogenic enzyme (fatty acid synthase and malic enzyme) activities were significantly increased by high fat diet. However, hepatic total lipid, triglyceride, total cholesterol and Serum GPT were significantly decreased by genistein intake. Also, genistein supplementation decreased serum total lipid, triglyceride, glucose and insulin concentration, hepatic lipogenic enzyme (fatty acid synthase and malic enzyme) activities. There were no differences by genistein level except for serum insulin. These results suggest that fatty liver induced by high fat diet was caused by increased serum lipid profiles and hepatic lipogenesis, whereas, genistein may be useful in inhibiting of fatty liver by reducing serum lipid profiles and hepatic lipogenesis.

• International Journal of Oral Biology
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• v.37 no.4
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• pp.189-195
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• 2012

Resistance to the induction of apoptosis is a possible mechanism by which tumor cells can survive anti-neoplastic treatments. Melanoma is notoriously resistant to anti-neoplastic therapy. Previous studies have demonstrated focal adhesion kinase (FAK) overexpression in melanoma cell lines. Given its probable role in mediating resistance to apoptosis, many researchers have sought to determine whether the downregulation of FAK in melanoma cells would confer a greater sensitivity to anti-neoplastic agents. Genistein is a known inhibitor of protein-tyrosine kinase (PTK), which may attenuate the growth of cancer cells by inhibiting the PTK-mediated signaling pathway. This present study was undertaken to investigate the effect of genistein on the expression of FAK and cell cycle related proteins in the G361 melanoma cell line. Genistein was found to have a preferential cytotoxic effect on G361 melanoma cells over HaCaT normal keratinocytes. Genistein decreased the expression of 125 kDa phosphotyrosine kinase and the FAK protein in particular. Genistein treatment did not affect the expression of p53 in G361 cells in which p21 is upregulated. The expression of cyclin B and cdc2 was downregulated by genistein treatment. Taken together, our data indicate that genistein induces the decreased proliferation of G361 melanoma cells via the inhibition of FAK expression and regulation of cell cycle genes. This suggests that the use of genistein may be a viable approach to future melanoma treatments.

• KSBB Journal
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• v.14 no.4
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• pp.490-494
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• 1999

This study was carried out to examine some factors affecting the supercritical carbon dioxide extraction of genistein from soybean. The factors investigated in this study were pressure, temperature, flow rate of carbon dioxide, and concentration of modifier. It was foumd out that genistein is not extracted in the absence of modifier. Ethanol was found to be more effective modifier than methanol. 70% of genistein was extracted at 35$^{\circ}C$, 300bar and ethanol 15% (w/v) as compared with the performances of organic solvent extraction.

• Clinical and Experimental Reproductive Medicine
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• v.40 no.2
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• pp.60-66
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• 2013

Objective: Impairment of spermatogenesis has been identified as an inevitable side effect of cancer treatment. Although estrogen treatment stimulates spermatogenic recovery from the impaired spermatogenesis by suppressing the intra-testicular testosterone (ITT) level, side effects of estrogen are still major impediments to its clinical application in humans. Soybeans are rich in genistein, which is a phytoestrogen that binds to estrogen receptors and has an estrogenic effect. We investigated the effects of genistein administration on ITT levels, testis weight, and recovery of spermatogenesis in rats treated with a chemotherapeutic agent, busulfan. Methods: Busulfan was administered intraperitoneally to rats, and then a GnRH agonist was injected subcutaneously into the back, or genistein was administered orally. Results: The weight of the testes was significantly reduced by the treatment with busulfan. The testis weight was partially restored after busulfan treatment by additional treatment with either the GnRH agonist or genistein. Busulfan also induced atrophy of a high percentage of the seminiferous tubules, but this percentage was decreased by additional treatment with either the GnRH agonist or genistein. Treatment with genistein was effective at suppressing and maintaining ITT levels comparable to that in the GnRH agonist group. Conclusion: Genistein effectively suppressed ITT levels and stimulated the recovery of spermatogenesis in rats treated with a chemotherapeutic drug. This suggests that genistein may be a substitute for estrogens, for helping humans to recover fertility after cancer therapy without the risk of side effects.

• Microbiology and Biotechnology Letters
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• v.36 no.1
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• pp.72-81
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• 2008

The effect of genistein on melanin synthesis was studied using in vitro and in vivo model. Genistein inhibited melanin synthesis in cultured melan-a cells dose dependently. Tyrosinase activity was decreased by genistein treatment in melan-a cells, but genistein did not inhibit tyrosinase directly. Genistein did not affect the expression of tyrosinase in melan-a cells. Genistein inhibited the activity of ${\alpha}$-glucosidase in virtro and the glycosylation of tyrosinase in melan-a cells. The resulting unsaturated glycosylation of tyrosinase makes it unstable and disturb correct transportation. To further clarify the effect of genistein on the melanogenesis, we established UVB-induced hyperpigmentation on the shaved backs of brown guinea pigs. The animals were exposed to UVB radiation once a week for three consecutive weeks. Genistein (1 and 2%) or vehicle alone as a control were then topically applied to the hyperpigmented areas daily. Genistein showed significant lightening effect on the UVB-induced hyperpigmentation in five weeks. Depigmenting effect was prominent in 2% genistein treatment with Fontana-Masson staining. In conclusion, genistein may be a useful agent for skin whitening.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.452-459
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• 2017

In this study, the effect of particle size of genistein-loaded solid lipid particulate systems on drug dissolution behavior and oral bioavailability was investigated. Genistein-loaded solid lipid microparticles and nanoparticles were prepared with glyceryl palmitostearate. Except for the particle size, other properties of genistein-loaded solid lipid microparticles and nanoparticles such as particle composition and drug loading efficiency and amount were similarly controlled to mainly evaluate the effect of different particle sizes of the solid lipid particulate systems on drug dissolution behavior and oral bioavailability. The results showed that genistein-loaded solid lipid microparticles and nanoparticles exhibited a considerably increased drug dissolution rate compared to that of genistein bulk powder and suspension. The microparticles gradually released genistein as a function of time while the nanoparticles exhibited a biphasic drug release pattern, showing an initial burst drug release, followed by a sustained release. The oral bioavailability of genistein loaded in solid lipid microparticles and nanoparticles in rats was also significantly enhanced compared to that in bulk powders and the suspension. However, the bioavailability from the microparticles increased more than that from the nanoparticles mainly because the rapid drug dissolution rate and rapid absorption of genistein because of the large surface area of the genistein-solid lipid nanoparticles cleared the drug to a greater extent than the genistein-solid lipid microparticles did. Therefore, the findings of this study suggest that controlling the particle size of solid-lipid particulate systems at a micro-scale would be a promising strategy to increase the oral bioavailability of genistein.

• Food Science and Biotechnology
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• v.17 no.5
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• pp.1021-1024
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• 2008

Genistein, one of the isoflavones in doenjang, is generally known to prevent various cancers, osteoporosis, climacterium, and menopause symptoms, and has better bioavailability and healthful physiological effects than its glucoside, genistin. In both traditional and commercial doenjangs, genistein content ranged from 370 to 1,510 mg/kg, however, significant amounts of genistin also existed at the level of 190 to 350 mg/kg. After treating with corn $\beta$-glucosidase, over 84% of genistin in doenjang was converted to genistein. However, physiochemical characteristics such as pH, viscosity, 2-thiobarbituric acid (TBA) value, and color were not changed significantly after corn $\beta$-glucosidase treatments. Therefore, this study shows that the improved doenjang with the increased genistein content can be produced using corn $\beta$-glucosidase.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.8
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• pp.1220-1225
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• 2008

This study was conducted to investigate the protective effect of genistein on the antioxidative defence system and membrane fluidity in chick skeletal muscle cells after supplementation with 0, 20, 40, and $80{\mu}mol/L$ genistein in $50{\mu}mol/L$ $FeSO_4/H_2O_2$ treated cells for 24 h. Genistein supplementation recovered the decreased activity of total superoxide dismutase induced by $FeSO_4/H_2O_2$, significantly increased glutathione peroxidase activity (p<0.05) and decreased malondialdehyde production (p<0.05). The treatment of 80 mol/L genistein in $FeSO_4/H_2O_2$ treated cells decreased the secretion of creatine kinase (p<0.05). Fluorescence polarization values and microviscosities observed with $FeSO_4/H_2O_2$ treated cells were significantly higher than those observed with no $FeSO_4/H_2O_2$ treated cells. The addition of $80{\mu}mol/L$ genistein improved the increased fluorescence polarization value (p<0.05) caused by $FeSO_4/H_2O_2$ treatment. The microviscosity value was significantly decreased by adding genistein (p<0.05). In conclusion, genistein protected skeletal muscle cells from oxidative damage by improving antioxidative status and membrane fluidity.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.759-764
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• 2013

Background: The high recurrence rate after hepatic resection in hepatocellular carcinoma (HCC) is a major obstacle to improving prognosis. The objective of the present study was to explore the function of genistein, a soy-derived isoflavone, in enhancing the inhibitory effect of cisplatin on HCC cell proliferation and on tumor recurrence and metastasis in nude mice after curative hepatectomy. Methods: Proliferation of human HCC cells (HCCLM3) was detected by 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide (MTT) assay. Synergistic effects of genistein and cisplatin were evaluated with the median-effect formula. Nude mice bearing human HCC xenografts underwent tumour resection (hepatectomy) 10 days post implantation, then received intraperitoneal administration of genistein or cisplatin alone or the combination of the two drugs. 33 days after surgery, recurrent tumours and pulmonary metastasis were evaluated individually. MMP-2 level in recurrent tumours was detected by immunohistochemistry and real-time PCR; MMP-2 expression in HCCLM3 was detected by immunocytochemistry. Results: Genistein and cisplatin both suppressed the growth and proliferation of HCCLM3 cells. The two drugs exhibited synergistic effects even at relatively low concentrations. In vivo, mice in the combined genistein and cisplatin group had a smaller volume of liver recurrent tumors and fewer pulmonary metastatic foci compared with single drug treated groups. Cisplatin upregulated the expression of MMP-2 in both recurrent tumours and HCCLM3, while genistein abolished cisplatin-induced MMP-2 expression. Conclusions: Genistein reinforced the inhibitory effect of cisplatin on HCC cell proliferation and tumour recurrence and metastasis after curative hepatectomy in nude mice, possibly through mitigation of cisplatin-induced MMP-2 upregulation.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.6
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• pp.579-589
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• 2017

Anesthetics are used extensively in surgeries and related procedures to prevent pain. However, there is some concern regarding neuronal degeneration and cognitive deficits arising from regular anesthetic exposure. Recent studies have indicated that brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are involved in learning and memory processes. Genistein, a plant-derived isoflavone, has been shown to exhibit neuroprotective effects. The present study was performed to examine the protective effect of genistein against isoflurane-induced neurotoxicity in rats. Neonatal rats were exposed to isoflurane (0.75%, 6 hours) on postnatal day 7 (P7). Separate groups of rat pups were orally administered genistein at doses of 20, 40, or 80 mg/kg body weight from P3 to P15 and then exposed to isoflurane anesthesia on P7. Neuronal apoptosis was detected by TUNEL assay and FluoroJade B staining following isoflurane exposure. Genistein significantly reduced apoptosis in the hippocampus, reduced the expression of proapoptotic factors (Bad, Bax, and cleaved caspase-3), and increased the expression of Bcl-2 and Bcl-xL. RT-PCR analysis revealed enhanced BDNF and TrkB mRNA levels. Genistein effectively upregulated cAMP levels and phosphorylation of CREB and TrkB, leading to activation of cAMP/CREB-BDNF-TrkB signaling. PI3K/Akt signaling was also significantly activated. Genistein administration improved general behavior and enhanced learning and memory in the rats. These observations suggest that genistein exerts neuroprotective effects by suppressing isoflurane-induced neuronal apoptosis and by activating cAMP/CREB-BDNF-TrkB-PI3/Akt signaling.