ライフサイエンスコーパス: apigenin

1 in part, the photochemopreventive effects of apigenin.

2 ee-living NGR234 cultured in the presence of apigenin.

3 on, along with an increase in sub-G1 peak by apigenin.

4 vities of both enzymes could be inhibited by apigenin.

5 racterize two CD38 inhibitors: quercetin and apigenin.

6 an BACE-1, better than the parent flavonoid, apigenin.

7 of UVB (300-1,000 J/m(2)), then treated with apigenin (0-50 micromol/L), and harvested to assess apop

8 he sunflower honey, while a larger amount of apigenin (0.97 mg/kg) was determined in the buckwheat ho

9 Apigenin (4', 5, 7,-trihydroxyflavone), a common dietary

10 s apigenin-6-C-galactoside-8-C-arabinoside & apigenin-6-C-arabinoside-8-C-galactoside, and 9,12,13-tr

11 ed to be L-tryptophan, Wessely-Moser isomers apigenin-6-C-galactoside-8-C-arabinoside & apigenin-6-C-

12 Apigenin 7-O-apiosylglucoside in celery leaves was resis

13 Apigenin 7-O-apiosylglucoside was converted to apigenin

14 idase-rich ingredients, but was converted to apigenin 7-O-glucoside at pH 2.7 when processed at 100 d

15 Apigenin 7-O-glucoside in chamomile extract was readily

16 Apigenin 7-O-glucoside showed little conversion or degra

17 igenin 7-O-apiosylglucoside was converted to apigenin 7-O-glucoside when heated at pH 3 and 100 degre

18 ganin, mussaenoside, luteolin 7-O-glucoside, apigenin 7-O-glucuronide and tricin 7-O-diglucuronide ha

19 affeoylquinic acid, 5-O-caffeoylquinic acid, apigenin 7-O-glucuronide in primary heads as well 1,5-di

20 uranetin 7-O-neohesperidoside (poncirin) and apigenin 7-O-neohesperidoside (rhoifolin).

21 idoside, 5.1 +/- 0.1mg/100g), and rhoifolin (apigenin 7-O-neohesperidoside, 2.0 +/- 0.1mg/100g).

22 nd quercetin glucuronide, and (iii) parsley: apigenin-7-apiosylglucoside (apiin) and isorhamnetin-3-O

23 the melon peels by 33.45mg/100g, followed by apigenin-7-glycoside (29.34mg/100g).

24 Apigenin-7-O-beta-d-glucuronide, caffeic and carnosic ac

25 The flavonoids luteolin-7-O-glucoside, apigenin-7-O-glucoside (cosmosiin), luteolin 3'-O-beta-d

26 hin, eriocitrin, rutin, apigenin, quercetin, apigenin-7-O-glucoside and kaempferol) were quantified u

27 ty was attributed to luteolin-7-O-glucoside, apigenin-7-O-glucoside, caffeicacid, myrecitin and phlor

28 We have tentatively identified apigenin-7-O-glucoside, luteolin-3-O-glucuronide, malony

29 The flavonoids apigenin-7-O-glycoside (1955.55 ng/mg) and luteolin-7-O-

30 7-O-neohesperidoside, 28.5 +/- 0.7 mg/100g), apigenin 8-C-neohesperidoside (16.9 +/- 0.1mg/100g), pon

31 cetin 6-C-neohesperidoside (isomargaritene), apigenin 8-C-neohesperidoside, and O-glycosides, such as

32 buting to antioxidant activity were DGPP and apigenin 8-C-neohesperidoside, which could be extracted

33 Apigenin, a common dietary flavonoid abundantly present

34 Consistent with this, we showed that apigenin, a dietary flavonoid that has been shown to inh

35 Apigenin, a flavonoid abundantly found in fruits and veg

36 identification of human cellular targets of apigenin, a flavonoid abundantly present in fruits and v

37 We investigated the effects of apigenin, a naturally occurring plant flavone, on prosta

38 nocytes, and this induction was inhibited by apigenin, a nonmutagenic bioflavonoid that has been show

39 ibitor U0126 had no effect and the flavonoid apigenin, a nonspecific inhibitor of ERK1/2 and COX-2, a

40 Apigenin, a selective CK2 inhibitor, diminishes interpha

41 e show that treatment of WEHI 231 cells with apigenin, a selective inhibitor of the protein kinase CK

42 etin, myricetin and gossypetin, and flavones apigenin, acacetin, luteolin, orientin and tricin, are s

43 , gallic acid, p-cumaric acid, sinapinic and apigenin acids were detected in Gemlik olive fruit.

44 Finally, apigenin administration to obese mice increases NAD(+) l

45 n chamomile extract was readily converted to apigenin aglycone after combination with almond, flax se

46 Apigenin also down-regulated STAT3 target genes MMP-2, M

47 state cancer cells with 10 and 20 micromol/L apigenin also increased protein levels of E-cadherin by

48 Apigenin also inhibits the increase in promoter activity

49 , a MEK inhibitor, and greatly attenuated by apigenin, an inhibitor of the Ras --> Raf --> MEK --> ER

50 and PLD2 enzymatic activity inhibitors (30nM apigenin and 300nM 5-fluoro-2-indolyl des-chlorohalopemi

51 nd the structurally related natural flavones apigenin and chrysin break TRAIL resistance in HTLV-1-as

52 Hence, only hydroxyl flavones, such as apigenin and chrysin, and flavonols, such as galangin, k

53 ncreases non-specific endonuclease activity, apigenin and epicatechin increase the excision of damage

54 specificity for flavones such as chrysin and apigenin and is responsible for biosynthesis of baicalei

55 In addition, exposure of apigenin and kaempferol to cultured hepatocytes, mimicki

56 of quercetin (3) and those of isorhamnetin, apigenin and luteolin (1).

57 in, kaempferol, and myricetin) and flavones (apigenin and luteolin) was assessed from food-frequency

58 Apigenin and quercetagetin demonstrated most significant

59 e that among the major flavonoids of citrus, apigenin and quercetagetin have potent anti-cancer activ

60 suggest that the change in Bax/Bcl2 ratio by apigenin and quercetagetin seems to be due to their abil

61 48h confirmed the induction of apoptosis by apigenin and quercetagetin.

62 cording to their major flavonoid (quercetin, apigenin and rutin) and phenolic (chlorogenic, caffeic a

63 fragmentation is reduced in the presence of apigenin and slightly increased by sakuranetin.

64 Results from these studies showed that apigenin and tt-farnesol may enhance the cariostatic eff

65 d with phenolic acids, flavone (luteolin and apigenin) and flavonol (quercetin) derivatives, which we

66 Furthermore, we show that wogonin, apigenin, and chrysin also enhance TRAIL-mediated apopto

67 ounds such as 3-(3-hydroxyphenyl)propionate, apigenin, and naringenin, were more abundant in the dry

68 In concert with these results, apigenin, and not baicalein, blocked the localization of

69 esveratrol (a major polyphenol in red wine), apigenin, and S17834 (a synthetic polyphenol), increased

70 cetoxypinoresinol, syringaresinol, luteolin, apigenin, and the hydrolysis products of oleuropein expr

71 Idf mutant produces highly reduced levels of apigenin- and tricin-related flavonoids, resulting in a

72 ease anti-tumor efficacy of the isoflavonoid apigenin (APG) in human malignant neuroblastoma SK-N-DZ

73 Apigenin (Api) and tt-farnesol (Far) are two naturally o

74 Ara h 8 binds the isoflavones quercetin and apigenin as well as resveratrol avidly.

75 tor, the flavonoid 4',5,7-trihydroxyflavone (apigenin), as well as RNA silencing, we found that the i

76 and derivatives and flavonoids (luteolin and apigenin), as well as tocopherols were quantified.

77 Instead we show that apigenin, as part of a non-canonical pathway, regulates

78 Three compounds, apigenin, baicalein, and quercetin, decreased Gli1 mRNA

79 cancer treatment and prevention abilities of apigenin, baicalein, curcumin, epigallocatechin 3-gallat

80 In the second protocol, administration of apigenin began 2 wk after tumor inoculation and continue

81 Apigenin binds to the C-terminal glycine-rich domain of

82 The selective CK2 inhibitor apigenin blocks proliferation of Wnt-1-transfected cells

83 reveal a novel anti-metastasis mechanism of apigenin but also support the notion that STAT3 is an at

84 ily hydroxylate position 6 of 7-O-methylated apigenin but not apigenin itself.

85 ene expression in an autoinductive loop, and apigenin, but not baicalein, treatment was associated wi

86 Oral intake of apigenin by gavage at doses of 20 and 50 microg/mouse/d,

87 hin-O-dihexoside, kaempferol-O-hexoside, and apigenin-C-hexoside-pentoside.

88 ), ferulic acid (6), grasshopper ketone (7), apigenin, cabraleone, chrysoeriol, 1beta,4beta-dihydroxy

89 luteolin 3'-O-beta-d-glucuronide, luteolin, apigenin, cirsimaritin, isokaempferide, penduletin, xant

90 els and that treatment of cell cultures with apigenin decreases global acetylation as well as the ace

91 psis cauline and senescing leaves accumulate apigenin, demonstrating that Arabidopsis plants have an

92 Additional studies show that the apigenin-dependent suppression of differentiation is ass

93 infusion were 5-O-caffeoylquinic acid and an apigenin derivative.

94 Using EMSA, we found that apigenin does not alter NF-kappaB-DNA binding activity i

95 cted to have anti-fibrotic activity; indeed, apigenin dose-dependently reduced collagen I in the huma

96 The absence of the catechol group on apigenin drastically decreased arginase inhibition.

97 oncentration-dependent neutrophil apoptosis (apigenin, EC=12.2 muM; luteolin, EC=14.6 muM; and wogoni

98 Our results indicate that apigenin effectively suppressed prostate carcinogenesis

99 Further study indicated that apigenin effectively suppressed STAT3 phosphorylation, d

100 P.o. administration of apigenin further resulted in increased levels of E-cadhe

101 ic and vanillic acids, and flavonoids, i.e., apigenin, genistein, hesperetin, kaempferol, luteolin, r

102 Among them, apigenin-glucuronide, lucenin-2 and lithospermic acid we

103 However, the anti-metastasis mechanism of apigenin has not been fully elucidated.

104 Taken together, these findings suggest that apigenin has strong potential for development as an agen

105 )), while minor compounds were caffeic acid, apigenin, hesperetin and naringenin.

106 ession of STAT3 or Twist1 partially reversed apigenin-impaired cell migration and invasion.

107 These findings reveal a novel role of apigenin in inhibiting HIF-1 and VEGF expression that is

108 Furthermore, the theoretical solubility of apigenin in the supercritical fluid system was obtained

109 rosmarinic) acids and flavones (luteolin and apigenin) in extracts from both sources.

110 rosmarinic acids) and flavones (luteolin and apigenin) in the polar extracts, with rosmarinic acid be

111 The results also demonstrate that apigenin-induced suppression of MUC1-C expression is ass

112 Apigenin inhibited expression of HIF-1alpha and VEGF via

113 In addition, apigenin inhibited the hyperphosphorylation of the pRb p

114 Apigenin inhibited tube formation in vitro by endothelia

115 We found that apigenin inhibited VEGF expression at the transcriptiona

116 Here we demonstrate that apigenin inhibits expression of vascular endothelial gro

117 In addition, our studies indicate that apigenin inhibits in vivo LPS-induced TNF and the mortal

118 Here, we report for the first time that apigenin inhibits the growth of androgen-responsive huma

119 In this study, we demonstrate that apigenin inhibits the production of proinflammatory cyto

120 NF-kappaB reporter constructs indicated that apigenin inhibits the transcriptional activity of NF-kap

121 We show that apigenin inhibits this response.

122 us study suggested that one pathway by which apigenin inhibits UV-induced and basal COX-2 expression

123 Apigenin intake by these mice also resulted in simultane

124 tro and in vivo growth inhibitory effects of apigenin involve modulation of IGF-axis signaling in pro

125 The dietary flavonoid apigenin is a bioactive compound that possesses low toxi

126 Apigenin is a nontoxic dietary flavonoid that has been s

127 Apigenin is a plant-derived flavanoid that has significa

128 atory cytokine production persists even when apigenin is administered after LPS stimulation.

129 osition 6 of 7-O-methylated apigenin but not apigenin itself.

130 Treatment of MCF7 cells with apigenin leads to a dose-dependent arrest at the G(2)/M

131 vanillic acid, p-cumaric acid, luteolin, and apigenin levels were greater in early harvested samples

132 tates, which correlated with elevated plasma apigenin levels.

133 3 correlated with increasing serum and tumor apigenin levels.

134 appaB inhibitor IkappaBalpha was observed in apigenin LPS-stimulated human monocytes.

135 es of flavonoids include the flavones (e.g., apigenin, luteolin), flavonols (e.g., quercetin, myricet

136 Apigenin, luteolin, and chrysoeriol were most stable at

137 e we investigate the ability of the flavones apigenin, luteolin, and wogonin to induce neutrophil apo

138 by flow cytometry following incubation with apigenin, luteolin, and wogonin.

139 eotide reversed these effects and attenuated apigenin-mediated inhibition of IRS-1 phosphorylation co

140 ermore, both RNAi-mediated TAF1 ablation and apigenin-mediated inhibition of the kinase activity of T

141 uR levels by small interfering RNA inhibited apigenin-mediated stabilization of COX-2 mRNA.

142 rs (greater activity than reference compound apigenin), most of which were unrelated in chemical stru

143 ested for their activity on SIRT6, including apigenin, naringenin, luteolin, and kaempferol.

144 ted the in vivo growth inhibitory effects of apigenin on androgen-sensitive human prostate carcinoma

145 phorylation conferring inhibitory effects of apigenin on IGF-signaling.

146 which is exemplified here by the effects of apigenin on the alternative splicing activity of hnRNPA2

147 mRNA stability, and the inhibitory effect of apigenin on UVB-induced luciferase reporter gene activit

148 Blocking CK2 activity in LNCaP cells with apigenin or 5,6-dichlorobenzimidazole riboside led to a

149 treatment of cells with MEK/ERK inhibitors (apigenin or PD98059) eliminated TH expression and the as

150 of CK2alpha via the pharmacologic inhibitor apigenin or upon transfection of a CK2 kinase-inactive s

151 ional regulation, another mechanism by which apigenin prevents COX-2 expression is through mediating

152 l characterization of AHR targeting PROTACS (Apigenin-Protac) designed to degrade and inhibit the AHR

153 and flavonoid (catechin, eriocitrin, rutin, apigenin, quercetin, apigenin-7-O-glucoside and kaempfer

154 sent study, we examine the mechanism whereby apigenin regulates normal human keratinocyte differentia

155 Apigenin, resveratrol, and piceatannol all induced Nrf2

156 levels of Nrf2, and this can be modulated by apigenin, resveratrol, and piceatannol.

157 rcritical CO2 (USC-CO2) extraction to obtain apigenin-rich extracts from Scutellaria barbata D.

158 ing reduced TIAR showed marked resistance to apigenin's ability to inhibit UVB-induced COX-2 expressi

159 identify C1QTNF2 as a potential mediator of apigenin's anti-fibrotic activity.

160 To identify proteins mediating apigenin's effect, we next overlapped a 122-gene signatu

161 r-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association,

162 ellocathecin-3-gallate, is also inhibited by apigenin, suggesting that the two chemopreventive agents

163 In the present study, we showed that apigenin suppressed murine melanoma B16F10 cell lung met

164 dings suggest a molecular mechanism by which apigenin suppresses inflammation and modulates the immun

165 Apigenin suppresses the 12-O-tetradeconylphorbol-13-acet

166 The 160 identified high-confidence candidate apigenin targets are significantly enriched in three mai

167 green procedure yielded 20.1% and 31.6% more apigenin than conventional SC-CO2 extraction and HRE, re

168 ot blocked by the casein kinase II inhibitor apigenin, the protein kinase C inhibitor GF109203X, or e

169 The ability of apigenin to enhance UVB-induced apoptosis may explain, i

170 domain led to a reduction in the ability of apigenin to enhance UVB-induced apoptosis.

171 We investigated the ability of quercetin and apigenin to modulate platelet activation and aggregation

172 f the bioflavonoid 4',5,7-trihydroxyflavone (apigenin) to mouse skin effectively reduces the incidenc

173 Apigenin-treated mice had significantly diminished weigh

174 Here, we found that apigenin treatment also increased COX-2 mRNA stability,

175 Apigenin treatment also resulted in down-modulation of t

176 Apigenin treatment also resulted in induction of apoptos

177 as a chemopreventive compound indicates that apigenin treatment alters the molecular events initiated

178 Apigenin treatment enhanced UVB-induced apoptosis >2-fol

179 ogenous COX-2 mRNA in 308 keratinocytes, and apigenin treatment increased their localization to cell

180 that enhancement of UVB-induced apoptosis by apigenin treatment involves both the intrinsic and extri

181 Further, apigenin treatment of LNCaP cells resulted in G1 arrest

182 f human keratinocytes to study the effect of apigenin treatment on UVB-induced apoptosis: HaCaT human

183 ted by UVB exposure; however, the effects of apigenin treatment on UVB-irradiated keratinocytes are n

184 The cell growth inhibition achieved by apigenin treatment resulted in a significant decrease in

185 In cell culture studies, apigenin treatment resulted in cell growth inhibition an

186 When keratinocytes were exposed to UVB, apigenin treatment stimulated changes in Bax localizatio

187 Continuous intake of apigenin up to 50 weeks by TRAMP mice significantly impr

188 In the first protocol, apigenin was administered for 2 wk before inoculation of

189 Apigenin was administered to mice by gavage at doses of

190 The flavonoid apigenin was among 9 top-ranked compounds predicted to h

191 Using this approach, the flavone apigenin was identified as an inhibitor of MUC1-CD dimer

192 The tumor inhibitory effect of apigenin was more pronounced in the first protocol of ex

193 PS-stimulated mouse macrophages treated with apigenin was overcome by the over-expression of IKKbeta.

194 Among flavonoids, genistein and apigenin were able to effectively displace resveratrol f

195 e effective than the analogues quercetin and apigenin when tested at a concentration fully consistent

196 ing proteins that are known to interact with apigenin, which identified C1QTNF2, encoding for Complem