ライフサイエンスコーパス: sulforaphane

1 ted GLs hydrolysis to yield health-promoting sulforaphane.

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

3 nt of glucoraphanin that is the precursor to sulforaphane.

4 ccharide-induced nitric oxide formation like sulforaphane.

5 hemoprevention of squamous cell carcinoma by sulforaphane.

6 etylation in colon cancer cells treated with sulforaphane.

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

8 o mitochondrial dysfunction and prevented by sulforaphane.

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

10 ay a critical role in apoptosis induction by sulforaphane.

11 promoter, was 800 times less effective than sulforaphane.

12 critical role in initiation of cell death by sulforaphane.

13 y either quinone-induced oxidative stress or sulforaphane.

14 the concentrations of both the oxidants and sulforaphane.

15 of brassinin with structural similarities to sulforaphane.

16 rsion of the inactive precursor to bioactive sulforaphane.

17 IM-timer-Nrf2 confirmed its stabilisation by sulforaphane.

18 to converting methylsulfinylalkyl ITCs like sulforaphane.

19 rotubule stabilizer, an antioxidant, or with sulforaphane.

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

21 and attractive option for the protection of sulforaphane.

22 hed for participants assigned to placebo and sulforaphane.

23 ASD patients in response to orally-delivered sulforaphane.

24 oli significantly increased the formation of sulforaphane.

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

26 0.21 (0.02, 0.40)] and vegetable intake with sulforaphane [0.30 (0.20, 0.47)], S-methylcysteine [0.23

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

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

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

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

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

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

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

34 mplex compared to the reference NQO1 inducer sulforaphane (- 8.26 versus - 5.08 kcal mol(-), respecti

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

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

37 Both sulforaphane, a chemopreventive isothiocyanate, and oxid

38 Sulforaphane, a compound with known atheroprotective eff

39 Sulforaphane, a constituent of many edible cruciferous v

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

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

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

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

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

45 Sulforaphane, a naturally occurring cancer chemopreventi

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

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

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

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

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

51 The multi-functional phytochemical sulforaphane affects many of the biochemical abnormaliti

52 Sulforaphane also induced transcription of a luciferase

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

54 Sulforaphane also prevented hyperglycemia-induced activa

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

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

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

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

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

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

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

62 (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-

63 NRF2 activators such as sulforaphane and bardoxolone methyl are already in clini

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

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

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

67 Dual treatment with sulforaphane and diarylpropionitrile, an estrogen recept

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

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

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

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

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

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

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

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

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

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

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

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

80 Sulforaphane and the analogue significantly induced (P <

81 Both sulforaphane and the analogue were identified as potent

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

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

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

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

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

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

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

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

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

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

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

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

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

95 2 and HAP1 with increasing concentrations of sulforaphane, benzyl isothiocyanate (BITC), and epigallo

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

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

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

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

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

101 50 and 60 degrees C significantly increased sulforaphane content (p<0.05), whilst blanching at 70 an

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

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

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

105 hat glucoraphanin metabolites (sulforaphane, sulforaphane cysteine, sulforaphane N-acetyl cysteine) a

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

107 The sulforaphane-dependent increases in specific activities

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

109 glucosinolate degradation products, such as sulforaphane derived from glucoraphanin.

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

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

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

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

114 Sulforaphane does not reduce the body weight or food int

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

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

117 of selected molecular markers in response to sulforaphane ex vivo treatment in PBMCs from healthy don

118 ur findings argue for clinical evaluation of sulforaphane for weight loss and obesity-associated meta

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

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

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

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

123 for monitoring pharmacodynamic responses to sulforaphane in both healthy and autistic humans, and pr

124 t with the BET inhibitor JQ1 synergized with sulforaphane in colon cancer cells and suppressed tumor

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

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

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

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

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

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

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

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

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

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

135 LY294002 also inhibited sulforaphane-induced Nrf2 nuclear translocation.

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

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

138 Finally, sulforaphane inhibits HDAC6 deacetylase activity, and th

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

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

141 in (via topical delivery of the Nrf2 inducer sulforaphane) involves the stimulation of Krt9 expressio

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

143 Sulforaphane is a phytochemical that has received attent

144 Sulforaphane is a promising chemopreventive agent that e

145 Sulforaphane is an activator of transcription factor NF-

146 Sulforaphane is an isothiocyanate derived from crucifero

147 Sulforaphane is an isothiocyanate that reduces hepatic g

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

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

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

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

152 Studies with sulforaphane+JQ1 in combination implicated a BET/BRD9 ac

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

154 High glucoraphanin and sulforaphane levels in eCO(2) treated sprouts improved t

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

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

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

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

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

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

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

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

163 olites (sulforaphane, sulforaphane cysteine, sulforaphane N-acetyl cysteine) and indole metabolites (

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

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

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

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

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

169 Interestingly, low levels of ineffective sulforaphane nitrile were detected and positively correl

170 cessing on the formation of sulforaphane and sulforaphane nitrile.

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

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

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

174 The effects of sulforaphane on multiple pathways of biochemical dysfunc

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

176 2 gene inducers, such as the isothiocyanate sulforaphane or a bis-2-hydroxybenzylideneacetone Michae

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

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

179 Sulforaphane protects ARPE-19 cells from oxidative injur

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

181 ysiological pathways that can be affected by sulforaphane: redox metabolism/oxidative stress; heat sh

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

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

184 he conclusion that the antiobesity effect of sulforaphane requires functional leptin receptor signali

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

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

187 ral isothiocyanate and potent NRF2 activator sulforaphane reverses diet-induced obesity through a pre

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

189 bundance of this gene operon correlated with sulforaphane serum concentration.

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

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

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

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

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

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

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

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

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

199 This review discusses (a) the efficacy of sulforaphane (SFN) and indole-3-carbinol (I3C)/3,3'-diin

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

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

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

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

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

205 Sulforaphane (SFN) has been reported to regulate signali

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

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

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

209 Sulforaphane (SFN) is a biologically active phytochemica

210 Sulforaphane (SFN) is a biologically important isothiocy

211 Sulforaphane (SFN) is a naturally occurring isothiocyana

212 Sulforaphane (SFN) is an important cancer preventive age

213 Sulforaphane (SFN) is an isothiocyanate from broccoli th

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

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

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

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

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

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

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

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

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

223 Sulforaphane (SFN), an effective cancer preventive agent

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

225 Sulforaphane (SFN), an isothiocyanate, protects macropha

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

227 estigate SFX-01, a stabilised formulation of sulforaphane (SFN), for its effects on breast CSC activi

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

229 C), phenethyl ITC (PEITC), erucin (ERN), and sulforaphane (SFN), incorporated in water and broccoli e

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

231 e, focused on investigation of the effect of sulforaphane (SFN)-rich broccoli sprouts (BSp) and witha

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

233 ylmethane (DIM), indole-3-carbinol (I3C) and sulforaphane (SFN).

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

235 Sulforaphane(SFN) and erucin(ERN) are isothiocyanates (I

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

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

238 h in the precursor to antioxidant-activating sulforaphane significantly ameliorated kidney injury in

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

240 Intraperitoneal administration of sulforaphane significantly reversed the suppression of N

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

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

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

244 ults suggest that glucoraphanin metabolites (sulforaphane, sulforaphane cysteine, sulforaphane N-acet

245 resistance to the weight-reducing effect of sulforaphane, supporting the conclusion that the antiobe

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

247 tabolically relevant tissues highlights that sulforaphane suppresses fatty acid synthesis while promo

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

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

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

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

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

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

254 Cabbage contains precursors of sulforaphane, the most active natural activator of Nrf2.

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

256 Sulforaphane thus represents an attractive option for th

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

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

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

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

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

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

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

264 Sulforaphane treatment also increases cleavage of procas

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

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

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

268 We hypothesized that sulforaphane treatment would lead to hyperacetylation of

269 eous response to clozapine, minocycline, and sulforaphane treatments.

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

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

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

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

274 These effects of sulforaphane were glutathione dependent.

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

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

277 muscle as the most notable site of action of sulforaphane whose peripheral NRF2 action signals to all