ライフサイエンスコーパス: sulforaphane

1 ccharide-induced nitric oxide formation like sulforaphane.

2 hemoprevention of squamous cell carcinoma by sulforaphane.

3 from binding to the AP-1 DNA binding site by sulforaphane.

4 o mitochondrial dysfunction and prevented by sulforaphane.

5 s, including NQO1 in B cells by the chemical sulforaphane.

6 ay a critical role in apoptosis induction by sulforaphane.

7 promoter, was 800 times less effective than sulforaphane.

8 critical role in initiation of cell death by sulforaphane.

9 rotubule stabilizer, an antioxidant, or with sulforaphane.

10 y either quinone-induced oxidative stress or sulforaphane.

11 the concentrations of both the oxidants and sulforaphane.

12 of brassinin with structural similarities to sulforaphane.

13 in a similar range as the positive control l-sulforaphane.

14 and attractive option for the protection of sulforaphane.

15 hed for participants assigned to placebo and sulforaphane.

16 oli significantly increased the formation of sulforaphane.

17 ed with a view to intensify the formation of sulforaphane.

18 ase inhibitor activity, hydroxyurea (HU) and sulforaphane.

19 nt of glucoraphanin that is the precursor to sulforaphane.

20 Sulforaphane [1-isothiocyanato-4-(methylsulfinyl)butane]

21 We have found that sulforaphane [(-)-1-isothiocyanato-(4R)-(methylsulfinyl)

22 cultured murine brain endothelial cells with sulforaphane (2.5 mum) increased nuclear accumulation of

23 ifier of thiols) and by UV spectroscopy with sulforaphane, 2,2'-dipyridyl disulfide and 4,4'-dipyridy

24 hyl isothiocyanate (3 and 1.5 mmol/kg diet), sulforaphane (3 and 1.5 mmol/kg diet), phenethyl isothio

25 We found that sulforaphane (4-methylsulfinylbutyl isothiocyanate), a n

26 e effects on behavior of daily oral doses of sulforaphane (50-150 micromol) for 18 wk, followed by 4

27 out (nrf2 -/-) mice treated with vehicle or sulforaphane (9 micromol/day for 1 week, p.o.) was gener

28 ells to quinone-induced oxidative stress and sulforaphane, a cancer-preventive isothiocyanate.

29 Both sulforaphane, a chemopreventive isothiocyanate, and oxid

30 Sulforaphane, a constituent of many edible cruciferous v

31 We have previously demonstrated that sulforaphane, a dietary isothiocyanate derived from its

32 he present study reports a novel response to sulforaphane, a highly promising anticancer constituent

33 ap1 by some highly reversible agents such as sulforaphane, a more sensitive screening assay was devel

34 In this study, we report that purified sulforaphane, a natural isothiocyanate found in crucifer

35 induction is brought about by treatment with sulforaphane, a natural product.

36 Sulforaphane, a naturally occurring cancer chemopreventi

37 tion factor NF-E2-related factor-2 (Nrf2) by sulforaphane, a naturally occurring compound present in

38 Here, we demonstrate that the addition of sulforaphane, a potent stimulator of antioxidant respons

39 Treatment with sulforaphane, a small-molecule activator of the transcri

40 Remarkably, combinations of exemestane and sulforaphane act highly synergistically, and this proper

41 lacking the nrf2 gene, did not benefit from sulforaphane administration.

42 Sulforaphane also induced transcription of a luciferase

43 Interestingly, sulforaphane also inhibited the AKT and mTOR survival pa

44 Sulforaphane also prevented hyperglycemia-induced activa

45 modulation of drug-metabolizing enzymes are sulforaphane, an aliphatic isothiocyanate, and brassinin

46 Timed administration of sulforaphane, an NRF2 activator, significantly blocked t

47 of PI3K inhibitors, followed by exposure to sulforaphane, an Nrf2 inducer.

48 hepatoma cells was found to be inducible by sulforaphane, an organic isothiocyanate that can transcr

49 Here we designed sulforaphane analogs with replacement of the reactive is

50 tural features important for high potency in sulforaphane analogs: the sulfoxide or keto group and it

51 On the basis of these results, the sulforaphane analogue can be regarded as a readily avail

52 (LOQ) were 0.993, 0.77mg/L and 2.35mg/L for sulforaphane and 0.997, 0.42mg/L, 1.29mg/L for indole-3-

53 ion-dependent disruption by inducers such as sulforaphane and bis(2-hydroxybenzylidene)acetone.

54 cJun) results in loss of sensitivity to both sulforaphane and diamide in electrophoretic mobility shi

55 analysis of nuclear proteins also shows that sulforaphane and diamide, both known to react with cyste

56 Dual treatment with sulforaphane and diarylpropionitrile, an estrogen recept

57 Neither oxidants (sulforaphane and diethyl maleate) nor reducing compounds

58 ent with the dietary chemopreventive agents, sulforaphane and green tea polyphenol, and that this red

59 obtained was possible the identification of sulforaphane and iberin nitrile that present known biolo

60 Among them, sulforaphane and indole-3-carbinol have attracted a lot

61 method for the simultaneous determination of sulforaphane and indole-3-carbinol in broccoli using UPL

62 The content of sulforaphane and indole-3-carbinol varied between 72+/-9

63 A quantitative determination of sulforaphane and its mercapturic derivatives, eicosanoid

64 the cells were pretreated with vitamin E or sulforaphane and N-acetylcysteine; samples included A2E-

65 on of Keap1-dependent degradation of Nrf2 by sulforaphane and oxidative stress.

66 eversible reaction between isothiocyanate of sulforaphane and sulfhydryl nucleophiles of Keap1 is kin

67 ts of thermal processing on the formation of sulforaphane and sulforaphane nitrile.

68 e by macrophages, whereas Nrf2 activation by sulforaphane and tert-butylhydroquinone with subsequent

69 Sulforaphane and the analogue significantly induced (P <

70 Both sulforaphane and the analogue were identified as potent

71 he potential of phenethyl isothiocyanate and sulforaphane and their conjugates as chemopreventive age

72 ive activity of phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates durin

73 hormetic phytochemicals such as resveratrol, sulforaphanes and curcumin might protect neurons against

74 or Bak knockout mice resisted cell death by sulforaphane, and (c) MEFs derived from Bax and Bak doub

75 r gene activity by tert-butylhydroxyanisole, sulforaphane, and beta-naphthoflavone.

76 itively regulated by tert-butylhydroquinone, sulforaphane, and hemin with responses comparable to thi

77 tent of total glucosinolates, glucoraphanin, sulforaphane, and myrosinase activity were determined.

78 to oxidative stress caused by treatment with sulforaphane, and the accumulation resulted from inhibit

79 Chemical inducers such as sulforaphane are known to react with Keap1 cysteine resi

80 to animals, but some isothiocyanates such as sulforaphane are potent anti-carcinogens that have preve

81 sprouts (containing either glucoraphanin or sulforaphane as the principal enzyme inducer) were highl

82 In addition, sulforaphane, as well as the analogue, increased glutath

83 persisted for several days after removal of sulforaphane before returning to control levels.

84 2 and HAP1 with increasing concentrations of sulforaphane, benzyl isothiocyanate (BITC), and epigallo

85 After culture and in vitro exposure to sulforaphane, BITC, or EGCG, the elevated GSTP1 mRNA exp

86 In complementary experiments, sulforaphane blocked benzo[a]pyrene-evoked forestomach t

87 by electrophiles such as the isothiocyanate sulforaphane can direct Nrf2 accumulation in the nucleus

88 We also found that the chemopreventive agent sulforaphane can target these DCIS stem-like cells, redu

89 tential was comparable to that observed with sulforaphane (concentration required to double the speci

90 50 and 60 degrees C significantly increased sulforaphane content (p<0.05), whilst blanching at 70 an

91 sothiocyanate, phenethyl isothiocyanate, and sulforaphane correlate well with their potencies of indu

92 ays in chondrocytes and to determine whether sulforaphane could block cartilage destruction in osteoa

93 nown PXR antagonists, such as coumestrol and sulforaphane, could also interact on the outer surface o

94 enetic approach or with the dietary compound sulforaphane decreased SOX9 and ALDH1, and reduced tumor

95 The sulforaphane-dependent increases in specific activities

96 ride), thereby resembling the isothiocyanate sulforaphane derived from broccoli.

97 There is preliminary evidence that sulforaphane, derived from glucoraphanin found in a numb

98 IF bound to phenethylisothiocyanate and to l-sulforaphane (dietary isothiocyanates derived from water

99 ired in the pathogen-induced accumulation of sulforaphane displayed attenuated programmed cell death

100 Neither quinone-induced oxidative stress nor sulforaphane disrupts association between Keap1 and Nrf2

101 d the formation of any significant levels of sulforaphane due to inactivated myrosinase.

102 We confirmed this by demonstrating that sulforaphane enhances HSP90 acetylation, thereby inhibit

103 drogen peroxide (H(2)O(2)) and phyto-oxidant sulforaphane further stimulated IRES(Nrf2)-mediated tran

104 ditions, the predicted response of 4.0 mumol sulforaphane/g dry matter was confirmed experimentally.

105 tly greater number of participants receiving sulforaphane had improvement in social interaction, abno

106 n hair follicles after Nrf2 activation using sulforaphane identified the modulation of phase II metab

107 was to assess whether activation of nrf2 by sulforaphane in human microvascular endothelial cells pr

108 Thus, the dual actions of sulforaphane in inhibiting Helicobacter infections and b

109 The presence of sulforaphane in the complexes was confirmed by FTIR and

110 Although the role of sulforaphane in the induction of the transcription facto

111 ored by an increase in ITCs and specifically sulforaphane in the plasma.

112 Activation of nrf2 by sulforaphane induced nuclear translocation of nrf2 and i

113 phagy represents a defense mechanism against sulforaphane-induced apoptosis in human prostate cancer

114 Thus, it is reasonable to postulate that sulforaphane-induced apoptosis is amplified by a decreas

115 The sulforaphane-induced autophagy was associated with up-re

116 ce exhibited even greater protection against sulforaphane-induced cytochrome c release, caspase activ

117 LY294002 also inhibited sulforaphane-induced Nrf2 nuclear translocation.

118 on of this sequence abrogated both basal and sulforaphane-inducible reporter activity.

119 idative stress and the chemopreventive agent sulforaphane inhibit Keap1-dependent ubiquitination of P

120 Finally, sulforaphane inhibits HDAC6 deacetylase activity, and th

121 Finally, intraperitoneal injections of sulforaphane into mice during active HSV infection reduc

122 ever, it is not known whether the effects of sulforaphane involve suppression of AR.

123 prolonged antioxidant protection provided by sulforaphane is a general phenomenon that is mediated th

124 Sulforaphane is a phytochemical that has received attent

125 Sulforaphane is a promising chemopreventive agent that e

126 Sulforaphane is an activator of transcription factor NF-

127 Sulforaphane is an isothiocyanate derived from crucifero

128 The mechanism of action of sulforaphane is believed to involve modifications of cri

129 this study, we show for the first time that sulforaphane is effective at reducing the multiplicity a

130 d that 4-methylsulfinylbutyl isothiocyanate (sulforaphane) is released by Arabidopsis (Arabidopsis th

131 iation model using a series of ARE inducers: sulforaphane, isoliquiritigenin, 15-deoxy-Delta12,14-pro

132 Isoliquiritigenin and sulforaphane, known ARE activators that target Keap1, we

133 se adaptive changes and the Nrf2 inducers DL-sulforaphane, lipoic acid, and curcumin all replicate th

134 rcinogen-treated control group to 0.3 in the sulforaphane low-dose group, 0.3 and 0.4 in the two sulf

135 ARPE-19 cells treated with sulforaphane maintained significantly higher redox ratio

136 ring ultrafiltration, a complete recovery of sulforaphane, malic acid and citric acid was achieved, w

137 Recent reports show that sulforaphane may impair prostate cancer growth through i

138 PPK onset, which can be prevented by topical sulforaphane-mediated activation of NRF2.

139 , suggesting that Bax and Bak might regulate sulforaphane-mediated induction of Apaf-1 protein.

140 an increase in the urinary concentrations of sulforaphane metabolites and vitamin C.

141 ate to severe ASD received the phytochemical sulforaphane (n = 29)--derived from broccoli sprout extr

142 ate-N-acetylcysteine (8 and 4 mmol/kg diet), sulforaphane-N-acetylcysteine (8 and 4 mmol/kg diet) dur

143 phane low-dose group, 0.3 and 0.4 in the two sulforaphane-N-acetylcysteine groups, and 0.4 in the phe

144 lung tumor incidences in groups treated with sulforaphane-N-acetylcysteine in the diet were also sign

145 nous enzyme myrosinase, sulforaphane (SF) or sulforaphane nitrile (SFN) are produced, depending on en

146 cessing on the formation of sulforaphane and sulforaphane nitrile.

147 The inactivation by sulforaphane of HDAC6-mediated HSP90 deacetylation and c

148 Dietary sulforaphane, of recognized low toxicity, was selected f

149 AC6 deacetylase activity, and the effects of sulforaphane on AR protein are abrogated by overexpressi

150 The effects of sulforaphane on multiple pathways of biochemical dysfunc

151 ucosinolate precursors) some of which (e.g., sulforaphane or 4-methylsulfinylbutyl isothiocyanate) ar

152 2 gene inducers, such as the isothiocyanate sulforaphane or a bis-2-hydroxybenzylideneacetone Michae

153 n rat brains following stroke, and show that sulforaphane pretreatment affects Nrf2 distribution in t

154 We also show that sulforaphane pretreatment is able to reduce the activity

155 Sulforaphane protects ARPE-19 cells from oxidative injur

156 Treatment with sulforaphane provided protection against a virulent H. a

157 Postinjury administration of sulforaphane reduced the loss of endothelial cell marker

158 Pretreatment with the Nrf2 inducer sulforaphane reduced total cellular Nrf2 levels in peri-

159 The treatment of ALL leukemic cells with sulforaphane resulted in dose-dependent apoptosis and G2

160 Exposure of PC-3 and LNCaP cells to sulforaphane resulted in several specific features chara

161 Topical application of sulforaphane-rich extracts of 3-day-old broccoli sprouts

162 Treatment with the natural chemical sulforaphane (SF) ameliorates skin blistering in keratin

163 In contrast, activation of Nrf2 by sulforaphane (SF) and tert-butylhydroquinone (tBHQ) depe

164 Sulforaphane (SF) or cinnamic aldehyde (CA) was administ

165 s of GR by the endogenous enzyme myrosinase, sulforaphane (SF) or sulforaphane nitrile (SFN) are prod

166 its chemopreventive ability in comparison to sulforaphane (SF), the ITC derived from broccoli.

167 cancer isothiocyanates-sulforaphene (SE) and sulforaphane (SF).

168 lls treated with the dietary isothiocyanate, sulforaphane (SFN) and carried out follow-up biological

169 Cancer chemopreventive agent sulforaphane (SFN) and dibenzoylmethane (DBM) showed ant

170 r, while covalent Keap1 modifiers, including sulforaphane (SFN) and dimethyl fumarate (DMF), are unab

171 Sulforaphane (SFN) and its N-acetyl-L-cysteine (NAC) con

172 nts or treatment with proteasomal activators sulforaphane (SFN) and mevalonolactone (MVA) ameliorated

173 dicate that natural isothiocyanates, such as sulforaphane (SFN) and phenethyl isothiocyanate (PEITC)

174 The Nrf2 inducer sulforaphane (SFN) as well as ectopic Nrf2 expression or

175 evidence that the oral administration of d,l-sulforaphane (SFN) can decrease the incidence or burden

176 Sulforaphane (SFN) has been reported to regulate signali

177 e (EGCG) in green tea polyphenols (GTPs) and sulforaphane (SFN) in broccoli sprouts (BSp) on neutrali

178 A new method was developed to determine sulforaphane (SFN) in honey using liquid chromatography

179 We show here that Nrf2 activation with sulforaphane (SFN) in vivo or in vitro increases express

180 Sulforaphane (SFN) is a biologically active phytochemica

181 Sulforaphane (SFN) is a biologically important isothiocy

182 Sulforaphane (SFN) is a naturally occurring isothiocyana

183 Sulforaphane (SFN) is an important cancer preventive age

184 Sulforaphane (SFN) is an isothiocyanate from broccoli th

185 The dietary phytochemical sulforaphane (SFN) is known for its anti-cancer properti

186 Sulforaphane (SFN) is the product of the enzymatic hydro

187 Sulforaphane (SFN), a compound found at high levels in b

188 We have shown previously that sulforaphane (SFN), a constituent of many edible crucife

189 Previously, we showed that sulforaphane (SFN), a naturally occurring cancer chemopr

190 Here we show that sulforaphane (SFN), a naturally occurring isothiocyanate

191 study shows that oral gavage of 6 mumol d,l-sulforaphane (SFN), a synthetic analogue of cruciferous

192 D,L-sulforaphane (SFN), a synthetic analogue of the broccoli

193 We also demonstrate that sulforaphane (SFN), an antioxidant, regulates Nrf2 activ

194 Sulforaphane (SFN), an effective cancer preventive agent

195 Sulforaphane (SFN), an isothiocyanate, is part of an imp

196 A Nrf2 activator, Sulforaphane (SFN), augmented Prdx6, catalase and GSTpi

197 omising ITCs, phenethyl ITCs (PEITC) and D,L-sulforaphane (SFN), have differential effects on dsRNA-m

198 enzyl-ITC (BITC), phenethyl-ITC (PEITC), and sulforaphane (SFN), inhibit carcinogenesis in animal mod

199 esis by phenethyl isothiocyanate (PEITC) and sulforaphane (SFN).

200 d age-matched wild-type (WT) mice were given sulforaphane (SFN, an Nrf2 activator) and its natural so

201 ced 1-isothiocyanato-4-methylsulfinylbutane (sulforaphane; SFN), a secondary metabolite in many cruci

202 imal change (<3.3%), whereas those receiving sulforaphane showed substantial declines (improvement of

203 ct glucoraphanin concentrations, and its ITC sulforaphane significantly increased during shelf life i

204 Intraperitoneal administration of sulforaphane significantly reversed the suppression of N

205 -butylhydroquinone, beta-naphthoflavone, and sulforaphane, significantly increased the GFP level in t

206 s also abolished the counteracting effect of sulforaphane, suggesting mediation by nrf2 and related i

207 cells with tert-butylhydroquinone (tBHQ) or sulforaphane (SUL), two potent phase II enzyme inducers,

208 Nrf2 activation via Keap1-KD or sulforaphane suppressed hormone-induced differentiation

209 A blanching step was designed to favor sulforaphane synthesis in broccoli.

210 A variety of oxidants, including sulforaphane, tert-butylhydroquinone, and H2O2, could ef

211 evels of glucoraphanin (the glucosinolate of sulforaphane) than do the corresponding mature plants.

212 to identify beta-mercaptoethanol adducts of sulforaphane that had been released from Keap1.

213 rated, using [(14)C]phenethyl ITC and [(14)C]sulforaphane, that NAC pretreatment significantly reduce

214 s for 24 h with 0-5 microM concentrations of sulforaphane (the powerful Phase 2 enzyme inducer isolat

215 h more rapid excretion of the isothiocyanate sulforaphane; therefore, individuals who have this genet

216 Sulforaphane thus represents an attractive option for th

217 damage while pharmacologic intervention with sulforaphane to induce brain Hp is linked to a reduction

218 Finally, the administration of sulforaphane to the ALL xenograft models resulted in a r

219 Topical application of the NRF2 activator sulforaphane to the footpad of Krt16-/- mice prevented t

220 Upon discontinuation of sulforaphane, total scores on all scales rose toward pre

221 The ratio for sulforaphane-treated cells after exposure to 0.64 mM H2O

222 At 1.2 mM H2O2, the redox ratio of sulforaphane-treated cells was 2.30 +/- 0.18 compared wi

223 Interestingly, sulforaphane treatment also caused a dose- and time-depe

224 Sulforaphane treatment also increases cleavage of procas

225 is based on the following observations: (a) sulforaphane treatment caused a dose- and time-dependent

226 We report here that sulforaphane treatment fails to activate NRF2 and preven

227 Additionally, sulforaphane treatment was found to be effective in redu

228 We hypothesized that sulforaphane treatment would lead to hyperacetylation of

229 ked inhibitor of apoptosis on treatment with sulforaphane was also observed.

230 Further, brief exposure to sulforaphane was bactericidal, and eliminated intracellu

231 hiles in complex matrixes that modify Keap1, sulforaphane was spiked into a cocoa extract, and LC-MS/

232 ood grade polymers for microencapsulation of sulforaphane was studied by a complex coacervation metho

233 These effects of sulforaphane were glutathione dependent.

234 his study, tert-butylhydroquinone (tBHQ) and sulforaphane were used as activators of this pathway.

235 ransient treatment with N-acetylcysteine and sulforaphane, which act to increase glutathione levels t