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Myricetin 杨梅素杨梅树皮素 80%，90%，98%

plantextract

2012/05/21

中药/天然药检测

Myricetin Increases Hepatic Peroxisome Proliferator-Activated Receptor α Protein Expression and Decreases Plasma Lipids and Adiposity in Rats

Myricetin is a flavonol, belong to the flavonoid in Flavonoids (polyphenols), found in many grapes, berries, fruits, vegetables, herbs, as well as other plants. It has been used as antioxidant to lower cholesterol, treat certain types of cancer, etc.

Health benefits
1. Anti cancers
In the investigation of dietary polyphenols as anticarcinogenic agents and the apoptotic effects of piceatannol and myricetin,found that apoptosis induced by piceatannol or myricetin occurs through an ROS-independent cell death pathway. In conclusion, piceatannol and myricetin synergistically induced apoptosis in HL-60 cells but not in HepG2 cells. These findings suggest that the potential anticarcinogenic properties of dietary polyphenols depend largely on the cell line used, according to “Selective apoptotic effects of piceatannol and myricetin in human cancer cells” by Morales P, Haza AI.(1)

2. Skin Cancer
In the affirmation of myricetin, a flavonol, found in many plants, including tea, berries, fruits, vegetables, and medicinal herbs and its chemopreventive effects on skin cancer found that myricetin was found to inhibit UVB-induced angiogenesis by targeting PI3-K in an SKH-1 hairless mouse skin tumorigenesis model. Raf kinase is a critical target for myricetin in inhibiting the UVB-induced formation of wrinkles and suppression of type I procollagen and collagen levels in mouse skin, according to “Myricetin is a potent chemopreventive phytochemical in skin carcinogenesis” by Kang NJ, Jung SK, Lee KW, Lee HJ.(2)

3. Colon cancer
In the research of Myricetin, a well known bioflavonoid and its protective effect on colon cancer found that Myricetin not only brought about significant decrease in the incidence of number of tumor bearing rats but also the tumor incidence. Myricetin supplementation significantly reduced liver TBARS. Further the anti oxidant enzymes like Catalase, Glutathione peroxidase and GSH were significantly rejuvenated following myricetin supplementation in a dose dependent manner, according to “Effect of myricetin on 1,2 dimethylhydrazine induced rat colon carcinogenesis” by Nirmala P, Ramanathan M.(3)

4. Pancreatic cancer
In the observation of the flavonoid myricetin and its effect on metastatic pancreatic cancer cell lines, found that myricetin resulted in tumor regression and decreased metastatic spread. Importantly, myricetin was non-toxic, both in vitro and in vivo, underscoring its use as a therapeutic agent against pancreatic cancer, according to the study of “Myricetin induces pancreatic cancer cell death via the induction of apoptosis and inhibition of the phosphatidylinositol 3-kinase (PI3K) signaling pathway” by Phillips PA, Sangwan V, Borja-Cacho D, Dudeja V, Vickers SM, Saluja AK.(4)

5. Antioxidant and cytotoxic activity
In the evaluation of extracted from plants containing phenolic compound, including flavonoid-galloyl glycoside [myricetin 3-O-(2',3'4'-tri-O-galloyl)-α-l-rhamnopyranoside] and theirs antioxidant and cytotoxic effect found that the methanol extract exhibited high antioxidant activity (SC(50) = 3.94 µg/ml), which is correlated with its phenolic content. The extract also showed cytotoxic activity against Hep G2 (IC(50) value 1.41 µg/ml) confirming its anticancer activity against hepatocellular carcinoma, according to the study of “Antioxidant and cytotoxic activity of polyphenolic compounds isolated from the leaves of Leucenia leucocephala” by Haggag EG, Kamal AM, Abdelhady MI, El-Sayed MM, El-Wakil EA, Abd-El-Hamed SS.(5)

6. Liver cancer
In the examination of study the mechanism of myricetin and its effect on the HepG-2 cell line found that Myricetin significantly inhibits the proliferation and induces the apoptosis of HepG-2 in a dose-dependent manner, which is accompanied with G2/M and S phase arrest. In addition, myricetin also increases the activation of caspase 3,9 and results in a depolarization and delta psi m collapse in a dose-dependent manner, according to “[Studies on mechanism of myricetin-induced apoptosis in human hepatocellular carcinoma HepG-2 cells].[Article in Chinese]” by Zhang X, Ling Y, Yu H, Ji Y.(6)

7. Synovial sarcoma cells
In observation of myricetin and its effect on the destruction cartilage and bone in RA joint found that Myricetin significantly decreased IL-1beta-induced production of IL-6 and MMP-1 in synovial cells. Moreover, myricetin diminished the phosphorylation of Jun NH2-terminal kinase (JNK) and p38 MAPK. These results suggest that myricetin reduces the production of MMP and IL-6 in SW982 cells by inhibiting (mitogen-activated protein kinases)MAPKs (JNK and p38), according to “Myricetin inhibits IL-1beta-induced inflammatory mediators in SW982 human synovial sarcoma cells” by Lee YS, Choi EM.(7)

8. Leukemia
In the comparison of the cytotoxic effect of 11 flavonoids on chronic myeloid leukemia (erythroblast crisis) K562 cells and peripheral blood mononuclear cells from healthy donors found that Baicalein and myricetin had a specific cytotoxic effect on leukemia cells, according to “Cytotoxic effect of flavonoids on leukemia cells and normal cells of human blood” byRomanouskaya TV, Grinev VV.(8)

9. Cell transformation
In the analyzing myricetin and its effect on cellular processes including cell growth, proliferation, and apoptosis found that myricetin inhibited Akt-mediated activator protein-1 (AP-1) transactivation, cyclin D1 expression and cell transformation. Overall, our results indicate that Akt is a direct target for myricetin to inhibit cell transformation, acccording to “Akt is a direct target for myricetin to inhibit cell transformation” by Kumamoto T, Fujii M, Hou DX.(9)

10. Esophageal cancer
In the investigation of flavones and flavonols and their effect on on esophageal squamous cell carcinoma cell line (KYSE-510) found that the cytotoxic potency of these compounds was in the order of: luteolin>quercetin>chrysin>kaempferol>apigenin>myricetin. . Flow cytometry and DNA fragmentation analysis indicated that the cytotoxicity induced by flavones and flavonols was mediated by G(2)/M cell cycle arrest and apoptosis, according to “Cytotoxicity of flavones and flavonols to a human esophageal squamous cell carcinoma cell line (KYSE-510) by induction of G2/M arrest and apoptosis’ by Zhang Q, Zhao XH, Wang ZJ.(10)

11. Antitumour and anti-inflammatory activities
In the observation of of flavonoids isolated from Byrsonima crass and its effect on mammary tumour cells LM2, found that almost all the samples showed inhibitory activity to the release of NO but not of TNF-alpha. Of all substances tested, flavonoids 2 (quercetin) and 6 (myricetin) may show promising activity in the treatment of murine breast cancer by immunomodulatory and antiproliferative activities, according to “Isolated flavonoids against mammary tumour cells LM2″ by Carli CB, de Matos DC, Lopes FC, Maia DC, Dias MB, Sannomiya M, Rodrigues CM, Andreo MA, Vilegas W, Colombo LL, Carlos IZ.(11)

12. Ovarian cancer
In the research of inverse associations with certain flavonoids or flavonoid subclasses (myricetin, kaempferol, quercetin, luteolin, and apigenin) and ovarian cancer risk, found that In analyses of each individual flavonoid, only intake of apigenin was associated with a borderline significant decrease in risk (RR, highest vs. lowest quintile = 0.79, 95% CI = 0.59-1.06; p-trend = 0.26), and this association was significant after adjustment for intake of the other 4 individual flavonoids (comparable RR = 0.72, 95% CI = 0.53-0.98; p-trend = 0.09), according to “Flavonoid intake and ovarian cancer risk in a population-based case-control study” byGates MA, Vitonis AF, Tworoger SS, Rosner B, Titus-Ernstoff L, Hankinson SE, Cramer DW.(12)

13. Prostate cancer
In the selection of several potential uPA inhibitors (antipain, leupeptin, folic acid, rosmarinic acid, lavendustin A, fisetin, myricetin, tolfenamic acid) and examination of theirs effects in prostate cancer found that a proper diet rich in uPA-inhibiting nutraceuticals might support the prevention of prostrate cancer and be a supportive tool in prostate cancer treatment, according to “Nutraceutical inhibitors of urokinase: potential applications in prostate cancer prevention and treatment” by Jankun J, Selman SH, Aniola J, Skrzypczak-Jankun E.(13)

14. Breast cancer
In study of red wine intake and its beneficial health effects on the proliferation of hormone-dependent breast cancer cells found that the estrogenic activity of PIC(piceatannol) and MYR(myricetin) might be considered at least as a potential factor in the association of red wine intake and breast tumors, particularly in postmenopausal women, according to “The red wine phenolics piceatannol and myricetin act as agonists for estrogen receptor alpha in human breast cancer cells” by Maggiolini M, Recchia AG, Bonofiglio D, Catalano S, Vivacqua A, Carpino A, Rago V, Rossi R, Andò S.(14)

15. Etc.

杨梅素是一种黄酮类，属于黄酮类化合物中的类黄酮（多酚），在许多葡萄，浆果，水果，蔬菜，药材，以及其他植物中发现。它已被作为抗氧化剂使用，以降低胆固醇，治疗某些类型的癌症等。

健康的好处
1。抗
癌症调查膳食茶多酚作为抗癌药物和piceatannol和杨梅的细胞凋亡的影响，发现piceatannol或杨梅素诱导细胞凋亡的发生，通过一个ROS独立的细胞死亡途径。总之，piceatannol和杨梅，但不是在HepG2细胞协同诱导HL-60细胞凋亡。这些结果表明，膳食多酚潜在的抗癌特性在很大程度上取决于使用的细胞线，根据“选择性在人类癌细胞凋亡的影响的piceatannol和杨梅”Haza人工智能。磷，莫拉莱斯（1）

2。皮肤癌
的杨梅肯定，在许多植物中，包括茶，浆果，水果，蔬菜，药材，其化学预防皮肤癌的效果发现，杨梅发现针对UVB诱导的血管生成抑制1黄酮，PI3- K在圣公会-1无毛小鼠皮肤肿瘤模型。Raf激酶抑制UVB诱导皱纹的形成和抑制型我胶原和小鼠皮肤中的胶原蛋白水平的关键目标是为杨梅，根据“杨梅素是一种有效的化学预防植物化学成分，在皮肤癌”，新泽西州，郑SK康，李利千瓦，黄建忠（2）

3。
杨梅素的研究，一个众所周知的生物类黄酮，其保护作用，对结肠癌结肠癌在发现，杨梅不仅带来发病率在荷瘤鼠的数量也显着减少肿瘤的发病率。杨梅补充显着降低肝脏TBARS的。进一步的抗氧化剂，酶喜欢过氧化氢酶，谷胱甘肽过氧化物酶和谷胱甘肽均显着振兴杨梅具有剂量依赖性的补充，根据“对1,2二甲基肼诱导的大鼠大肠癌变的杨梅”涅玛拉磷，拉马纳坦研究（3）

4。胰腺癌
黄酮Myricetin和转移性胰腺癌细胞株的效果观察，发现杨梅，导致肿瘤缩小，降低转移扩散。重要的是，杨梅是无毒的，无论是在体外和体内，强调其作为对胰腺癌的治疗剂的使用，根据研究“杨梅素诱导胰腺癌细胞死亡，通过诱导细胞凋亡和抑制磷酸肌醇3 -激酶（PI3K）信号通路的“菲利普斯扩音，Sangwan至五，博尔哈-Cachoð，Dudeja至五，维克斯SM，萨鲁佳的AK。（4）

5。抗氧化和细胞毒活性
在含有酚类化合物的植物，包括类黄酮，没食子酰苷提取杨梅素3-O-（2'，3'4'-三-O-没食子酰基）-α-L-鼠李]，他们的评价抗氧化和细胞毒作用的发现，甲醇提取物具有较高的抗氧化活性（SC（50）= 3.94微克/毫升），这是其酚含量相关。提取物也表现出对Hep G2细胞的细胞毒活性（IC（50）值1.41微克/毫升），确认其对肝癌细胞的抗癌活性，按照“从Leucenia合欢的叶子中分离的多酚化合物的抗氧化和细胞毒活性”的研究哈加格的EG，卡迈勒上午，Abdelhady MI，厄尔尼诺-赛义德的MM，EL-瓦基勒的EA，阿布杜拉EL-哈米德SS（5）

6。
自学考试在肝癌的杨梅和其作用机制，对HepG-2细胞的发现，杨梅显着抑制增殖和诱导肝癌HepG-2细胞凋亡剂量依赖性，这是与G2 / M期的陪同下行和S期阻滞。此外，杨梅还增加了活化的caspase 3,9和剂量依赖的方式去极化和三角洲PSI米崩溃的结果，根据“杨梅素诱导人肝癌HepG-2细胞凋亡的机制[研究] [文章]中国“由张X，凌云，于吉华（6）

7。滑膜肉瘤细胞，
在杨梅和其上的破坏在RA关节软骨和骨的效果观察发现，杨梅素显着降低IL-1β诱导的滑膜细胞中IL-6和MMP-1的生产。此外，杨梅减少Jun氨基末端激酶（JNK）和p38的磷酸化。这些结果表明，杨梅降低生产通过抑制SW982细胞基质金属蛋白酶和IL-6（丝裂原活化蛋白激酶）激酶（JNK及p38），根据“杨梅素抑制IL-1β诱导的炎症介质，在SW982人类滑膜肉瘤细胞“，由李渝生，蔡的EM（7）

8。白血病
在11个黄酮类化合物的慢性粒细胞白血病（红细胞危机）K562细胞和外周血单核细胞从健康的捐赠者发现，黄芩素和杨梅素对白血病细胞的细胞毒作用，有一个特殊的细胞毒作用的比较，根据“黄酮类化合物的细胞毒作用对白血病细胞和正常细胞，人体血液“byRomanouskaya电视，Grinev维维。（8）

9。细胞转化
杨梅和细胞过程，包括细胞生长，增殖和凋亡的影响分析发现，杨梅抑制Akt蛋白介导激活蛋白-1（AP-1）的转录，细胞周期蛋白D1的表达和细胞转化。总的来说，我们的结果表明，Akt是抑制细胞转化为杨梅的直接目标，acccording“Akt的直接目标是为杨梅，抑制细胞转化”由熊T，藤井男，侯的DX（9）

10。食管癌
在食管鳞状细胞癌的细胞株（KYSE-510）上的黄酮和黄酮醇及其效果的调查发现，这些化合物的细胞毒性效力的顺序是：木犀草素>槲皮素>白杨>山奈酚>芹菜>杨梅。。流式细胞仪和DNA片段分析表明，黄酮和黄酮醇诱导的细胞毒性介导的G（2）/ M细胞周期阻滞和凋亡，根据“黄酮和黄酮一个人食管鳞状细胞癌的细胞株的细胞毒性（KYSE 510）通过诱导G2 / M期阻滞和细胞凋亡（10张旗，赵红，王之钧。“）

11。抗癌及抗发炎的活动，
从Byrsonima粗鲁和对乳腺肿瘤细胞的效果LM2分离黄酮的观察，发现，几乎所有的样本显示抑制活性，NO的释放，但TNF-α。测试的所有物质，黄酮类化合物（槲皮素）和6（杨梅）可能会显示在治疗小鼠乳腺癌的免疫调节和抗增殖活动的有前途的活动，根据“隔离黄酮LM2对乳腺肿瘤细胞的”卡利CB，德马托斯直流洛佩斯的FC，马亚直流，迪亚斯MB，三宫罗德里格斯厘米，Andreo马，Vilegas W，科伦坡的LL，卡洛斯工业区（11）

12。卵巢癌，
在某些黄酮或黄酮类的子类（杨梅素，山柰酚，槲皮素，木犀草素，芹菜素）和卵巢癌的风险与逆协会的研究发现，在每一个人的黄酮类化合物的分析，芹菜的摄入量只有边缘显著相关减少危险度（RR，最高与最低的五分之一= 0.79，95％CI = 0.59-1.06，P趋势= 0.26），与此关联的摄入量的调整后，其他4个人类黄酮（相当于RR = 0.72显着， 95％CI = 0.53-0.98; P-趋势= 0.09），根据“类黄酮的摄入量和卵巢癌的风险，在一个人口为基础的病例对照研究”byGates马，Vitonis自动对焦，Tworoger SS，罗斯纳乙，提图斯Ernstoff大号汉金森SE，克拉默德国之声（12）

13。前列腺癌
在几个潜在的尿激酶抑制剂的选择（antipain，亮肽素，叶酸，迷迭香酸，lavendustin一个，漆黄素，杨梅，tolfenamic酸）和他们的作用在前列腺癌的审查发现，适当的饮食丰富抑制UPA-营养品可能支持，Aniola塞尔曼的SH Jankun J，J，Skrzypczak-Jankun E.预防前列腺癌，并在治疗前列腺癌的辅助工具，根据：“保健品的尿激酶抑制剂在前列腺癌的预防和治疗中的应用潜力”（ 13）

14。
红酒摄入量和它的发现，雌激素活性的PIC（piceatannol）和马币（杨梅）可能会考虑至少在该协会的潜在因素的激素依赖性乳腺癌细胞增殖的保健功效研究乳腺癌红酒摄入量与乳腺癌肿瘤，特别是在绝经后妇女，根据“红酒酚piceatannol和杨梅的行为在人类乳腺癌细胞雌激素受体α激动剂”，Bonofiglio Maggiolini男，雷基亚公司D，卡塔拉诺小号，Vivacqua一，Carpino一，五，罗西ŕ罗岛，安藤S.（14）

相关话题

plantextract

第1楼2012/05/21

liqingliang_2008[at]yahoo.com.cn (Please change[at]to @)
herbextracts[at]yahoo.ca(Please change[at]to @)

0

梧桐

第2楼2012/05/25

楼主可以介绍一些这类成分从中药中的提取分离工艺或者质量控制方法就更好了

0

xiaowang268

第3楼2012/05/26

有些实验过程就好些

0

xiaowang268

第5楼2012/08/20

杨梅素的作用还是很好的

0

plantextract

第6楼2012/12/14

email:
liqingliang_2008[at]yahoo.com.cn (Please change[at]to @)
herbextracts[at]yahoo.ca(Please change[at]to @)

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