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1 Breast cancer and flavonoids - a role in prevention. Takemura H1, Sakakibara H, Yamazaki S, Shimoi K. Author information Institute for Environmental Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan. [email protected]. Abstract Endogenous estrogens, such as 17β-estradiol (E2), are implicated in the development of breast cancer. The putative mechanisms by which estrogens exert the carcinogenic effects have been recognized to involve the redox cycling of estrogen metabolites and subsequent estrogen-DNA adduct formation as well as the estrogen receptor-dependent pathway of estrogen-induced cell growth. The former pathway is regulated by phase I enzymes, mainly cytochrome P450 (CYP) 1A1, 1A2, and 1B1. Among them, CYP1B1 predominantly catalyzes the C4-position of E2 and forms carcinogenic 4-hydroxy-E2 (4-OHE2), whereas CYP1A1 and CYP1A2 convert E2 to non-carcinogenic-hydroxy-E2. Formed 4-OHE2 is further oxidized to semiquinones and quinones, which form DNA adducts, leading to mutagenic lesions. Consequently, CYP1B1 is highly expressed, and 4-OHE2 is predominantly detected in estrogen target neoplastic tissues. Moreover, invasion and metastasis are also involved in the development of breast cancer. Epidemiological studies suggest an inverse association between a higher intake of flavonoids and breast cancer risk. Flavonoids, which are widely distributed in the plant kingdom, have been recently reported as candidate compounds that can exert chemo preventive effects in estrogendependent or independent breast cancer. In this review, we provide a comprehensive overview of breast cancer and chemoprevention by flavonoids, mainly focusing on ER-mediated hormonal regulation, redox cycling of estrogen metabolites, and selective inhibition of CYP1B1. ----------------------------------------------------------------------------------------------- Green Tea (Flavanols content) One study looked at 472 women in various stages of breast cancer (labeled 1, II, or III, depending on how far the cancer had progressed). Increased green-tea consumption was associated with a decreased risk of lymph node metastasis in premenopausal women with stages I and II cancer. The researchers also found that if women with these stages of breast cancer consumed 5 cups a day of green tea on a longterm basis, they were more likely to be in remission 6 months later when the follow-up study was done. - The Natural Physician's Healing Therapies by Mark Stengler, N.D. ( Available on Amazon.com) 2 In test tube studies, green tea shut down the tumor promoters involved in breast cancer. Green tea inhibits the formation of cancer-causing agents in the stomach, including nitrosamines. The anticancer properties of green tea include: Immune stimulant. Inhibits platelet adhesion, and possibly metastasis. Antioxidant which protects immune cells for a higher tumor kill rate while protecting the valuable prostaglandin PGE-1. Inhibits metastasis. Inhibits the breakdown of connective tissue via collagenase, which is the primary mechanism for the spreading of cancer cells. - Beating Cancer with Nutrition by Patrick Quillin, PhD,RD,CNS - Available on Amazon.com http://www.naturalnews.com/025687_green_tea_breast_cancer.html#ixzz4DwnMBBHV Antitumor activity of the novel flavonoid Oncamex in preclinical breast cancer models British Journal of Cancer (2016) 114, 905–916. doi:10.1038/bjc.2016.6 www.bjcancer.com Published online 31 March 2016 Authors: Carlos Martínez-Pérez, Carol Ward, Arran K Turnbull, Peter Mullen, Graeme Cook, James Meehan, Edward J Jarman, Patrick IT Thomson, Colin J Campbell, Donald McPhail, David J Harrison & Simon P Langdon ------------------------------------------------------------------------------------------------------------------------------Myricetin research study Myricetin as the active principle of Abelmoschus moschatus to lower plasma glucose in streptozotocin-induced diabetic rats. Planta Med. 2005. Department of Pharmacy, Tajen Institute of Technology, Yen-Pou, Ping Tung Shien, Taiwan,. The antihyperglycemic action of myricetin, purified from the aerial part of Abelmoschus moschatus (Malvaceae), was investigated in streptozotocin-induced diabetic rats. These results suggest that myricetin has an ability to enhance glucose utilization to lower plasma glucose in diabetic rats lacking insulin. Anti-inflammatory health use Anti-inflammatory Activity of Myricetin Isolated from Myrica rubra Sieb. et Zucc. Leaves. Planta Med. 2010. Department of Pharmaceutics, Shenyang Pharmaceutical University, Shenyang, PR China. 3 MYRICA RUBRA leaves are commonly used in folk medicine to treat inflammatory disorders in China. Present studies on the anti-inflammatory effect of myricetin from MYRICA RUBRA Sieb leaves was evaluated with various IN VIVO models of both acute and chronic inflammations such as xylene-induced ear edema, acetic acid-induced vascular permeability, carrageenan-induced paw edema, leukocyte migration assay, and cotton pellet granuloma models. Myricetin showed a significant inhibition on ear edema and hind paw edema caused by xylene and carrageenan, respectively. Our results also support the claims of traditional Chinese medicine practitioners about the use of MYRICA RUBRA leaves in the treatment of inflammatory diseases. Inhibition of interleukin-12 production in mouse macrophages via decreased nuclear factorkappaB DNA binding activity by myricetin, a naturally occurring flavonoid. Arch Pharm Res. 2005. Pharmacological inhibition of interleukin-12 (IL-12) production may be a therapeutic strategy for preventing the development and progression of disease in experimental models of autoimmunity. In this study, the effects of myricetin, a naturally occurring flavonoid present in fruits, vegetables and medicinal herbs, on the production of IL-12 were investigated in mouse macrophages stimulated with lipopolysaccharide (LPS). Myricetin significantly inhibited the LPSinduced IL-12 production from both primary macrophages and the RAW264.7 monocytic cellline in a dose-dependent manner. The effect of myricetin on IL-12 gene promoter activation was analyzed by transfecting RAW264.7 cells with IL-12 gene promoter/luciferase constructs. Furthermore, activation of macrophages by LPS resulted in markedly enhanced binding activity to the NF-kappaB site, which significantly decreased upon addition of myricetin, indicating that myricetin inhibited IL-12 production in LPS-activated macrophages via the down-regulation of NF-kappaB binding activity. --------------------------------------------------------------------------------------------------------------------------- Cancer protection Life Sci. 2015. Molecular mechanisms underlying anticancer effects of myricetin. Dietary guidelines published in the past two decades have acknowledged the beneficial effects of myricetin, an important and common type of herbal flavonoid, against several human diseases such as inflammation, cardiovascular pathologies, and cancer. An increasing number of studies have shown the beneficial effects of myricetin against different types of cancer by modifying several cancer hallmarks including aberrant cell proliferation, signaling pathways, apoptosis, angiogenesis, and tumor metastasis. Most importantly, myricetin interacts with oncoproteins such as protein kinase B (PKB) (Akt), Fyn, MEK1, and JAK1-STAT3 (Janus kinase-signal transducer and activator of transcription 3), and it attenuates the neoplastic transformation of cancer cells. 4 Dietary flavonoids as proteasome inhibitors and apoptosis inducers in human leukemia cells. Biochem Pharmacol. 2005. The Prevention Program, Barbara Ann Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, MI It has been shown that proteasome activity is required for cancer cell survival and consumption of fruits and vegetables is associated with decreased cancer risk. In this study, we examined the flavonoids quercetin, apigenin, myricetin, and kaempferol for their proteasome-inhibitory and apoptosis-inducing abilities in human tumor cells. We report that apigenin and quercetin are much more potent than kaempferol and myricetin at: (i) inhibiting chymotrypsin-like activity of purified 20S proteasome and of 26S proteasome in intact leukemia Jurkat T cells; (ii) accumulating putative ubiquitinated forms of two proteasome target proteins, Bax and Inhibitor of nuclear factor kappabeta-alpha in Jurkat T cells and (iii) inducing activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase in Jurkat T cells. The proteasomeinhibitory abilities of these compounds correlated with their apoptosis-inducing potencies. Results from computational modeling of the potential interactions of these flavonoids to the chymotrypsin site (beta5 subunit) of the proteasome were consistent with the obtained proteasome-inhibitory activities. We found that the C (4) carbon may be a site of nucleophilic attack by the OH group of N-terminal threonine of proteasome beta5 subunit and that the C(3) hydroxyl may alter the ability of these flavonoids to inhibit the proteasome. Finally, apigenin neither effectively inhibited the proteasome activity nor induced apoptosis in non-transformed human natural killer cells. Our results suggested that the proteasome may be a target of these dietary flavonoids in human tumor cells and that inhibition of the proteasome by flavonoids may be one of the mechanisms responsible for their cancer-preventive effects. Myricetin Induces Cell Death of Human Colon Cancer Cells via BAX/BCL2-Dependent Pathway. Anticancer Res. 2014 Feb. Diabetes J Med Food. 2013. Effect of Emulin on blood glucose in type 2 diabetics. Emulin is a patented blend of chlorogenic acid, myricetin, and quercetin ( myricetin and quercetin are naturally ingredients content in each Flavanoplus blends) that has shown efficacy in reducing midday and post-oral glucose tolerance test (OGTT) area under the curve (AUC) glucose in streptozotocintreated rats. This human trial results suggest that Emulin, if consumed regularly, could not only have the acute effect of lowering the glycemic impact of foods, but chronically lower background blood glucose levels of type 2 diabetics. 5 Estrogenic effect Toxicol Lett. January 29 2014. The estrogenic effects of apigenin, phloretin and myricetin based on uterotrophic assay in immature Wistar albino rats. Chemicals that occur in vegetal food and known as phytoestrogens, because of their structures similarity to estrogen, have benefits on chronic diseases. Despite this, when they are taken at high amounts, they can cause harmful effects on endocrine system of human and animals. In this study, it has been intended to determine the estrogenic potencies of phytoestrogens apigenin, phloretin and myricetin whose affinities for estrogen receptors in vitro. The female rats divided into 17 groups, each containing 6 rats. There was a negative control group and there were positive control dose groups which contains ethinyl estradiol, ethinyl estradiol+tamoxifen and genistein. The other dose groups which were tested for estrogenic activity contains apigenin, myricetin and phloretin All chemicals have been given to Wistar immature female rats with oral gavage for 3 consecutive days. By using uterotrophic analysis, uterus wet and blotted weights, vaginal opening, uterus length of female rats has been recorded at the end of the experiment. For detect of cell response, luminal epithelium height, gland number and lactoferrin intensity in luminal epithelium of uterus were evaluated. Biochemical analysises in blood were performed. Relative uterus weights of rats in 100mg/kg/day dose group of myricetin were statistically increased according to vehicle control and positive control groups. In dose groups of apigenin and phloretin it was found that there were cell responses in uterus. All treatment groups had a significant difference in the high intensity of lactoferrin and uterine gland count compared to oil control group. There was no difference between phloretin and apigenin treatment groups in uterine weight statictically. Uterine heights were increased in positive control groups and 100mg/kg/day dose group of myricetin. Epithelial cell heights were increased in treatment groups except apigenin and phloretin dose groups. There was no difference between all treatment groups in vaginal opening values according to positive control. Sleep influence Biochem Biophys Res Commun. 2013 Oct 18. The flavonoid myricetin reduces nocturnal melatonin levels in the blood through the inhibition of serotonin N-acetyltransferase. Preformed beta-amyloid fibrils are destabilized by coenzyme Q10 in vitro. Biochem Biophys Res Commun. 2005. Inhibition of the formation of beta-amyloid fibrils (fAbeta), as well as the destabilization of preformed fAbeta in the CNS, would be attractive therapeutic targets for the treatment of Alzheimer's disease. We reported previously that nordihydroguaiaretic acid (NDGA) and winerelated polyphenol, myricetin, inhibit fAbeta formation from Abeta and destabilize preformed fAbeta in vitro. Using fluorescence spectroscopic analysis with thioflavin T and electron 6 microscopic studies, we examined the effects of coenzyme Q10 (CoQ(10)) on the formation, extension, and destabilization of fAbeta at pH 7.5 at 37 degrees C in vitro. We next compared the anti-amyloidogenic activities of CoQ10 with NDGA and myricetin. Coenzyme Q10 dosedependently inhibited fAbeta formation from amyloid beta-peptide (Abeta), as well as their extension. Moreover, it destabilized preformed fAbetas. The anti-amyloidogenic effects of Coenzyme Q10 were slightly weaker than those of NDGA and myricetin. Coenzyme Q10 could be a key molecule for the development of therapeutics for Alzheimer's disease. Anthocyanins, Flavanols, and free radical scavenging activity of Chinese bayberry (Myrica rubra) extracts and their color properties and stability. J Agric Food Chem. 2005. Characterization of anthocyanins and flavonols and radical scavenging activity assays of extracts from four Chinese bayberry (Myrica rubra) varieties with different fruit colors were carried out. One dominant anthocyanin and three major flavonols were isolated by HPLC, and cyanidin-3-Oglucoside and two of three flavonols, myricetin and quercetin-3-O-rutinoside, were identified by clochromatography with authentic standards. Both DPPH* and ABTS*(+) cation assays indicated that the black varieties (Biji and Hunan) demonstrated much higher radical scavenging activities than the pink (Fenhong) and yellow (Shuijing) varieties, which may be attributed to much higher levels of anthocyanins, flavonoids, and total phenolics in the black varieties. Myricetin inhibits matrix metalloproteinase protein expression and enzyme activity in colorectal carcinoma cells. Mol Cancer Ther. 2005. Because the activation of matrix metalloproteinases (MMP) is a key factor in the metastatic process of colon cancer, agents with the ability to inhibit MMP activity have potential in the treatment of colorectal carcinoma. In the present study, among 36 flavonoids examined, myricetin was found to be the most potent inhibitor of MMP-2 enzyme activity in COLO 205 cells. Results of the present study indicate that myricetin significantly blocked both endogenous and TPA-induced MMP-2 enzyme activity by inhibiting its protein expression and enzyme activity. The blockade involved suppression of PKC translocation, ERK phosphorylation, and cJun protein expression. Cactus Botanic introduces Myricetin extracted from Bayberry Bark Myricetin is a flavonoid that is commonly found in natural food sources such as berries, vegetables, teas, wine and herbs. Myricetin is considered to be an antioxidant, which means that it is capable of eliminating free radicals within the body. It is usually taken from the bark, leaves, and roots of the plant known as myrica cerifera, and is completely water soluble, which means it makes an excellent source for teas. Cactus Botanics introduces Myricetin 80%, tested by HPLC. -------------------------------------------------------------------------------------------------------------------------------