ライフサイエンスコーパス: curcumin

1 -MOFs and the phenolic hydroxyl group of the curcumin.

2 developed and used as delivery vehicles for curcumin.

3 butes to the anti-inflammatory properties of curcumin.

4 These nanocapsules can be conjugated with curcumin.

5 rstanding the polypharmacological effects of curcumin.

6 ws that the Abeta42 fibrils are disrupted by curcumin.

7 ng modifies the anti-cancerogenic effects of curcumin.

8 d beta(1-42) (Abeta42) aggregates induced by curcumin.

9 d more bioavailable compared to unformulated curcumin.

10 cyclodextrin and the aromatic rings group of curcumin.

11 derlie the inhibition of mPGES-1 and 5-LO by curcumin.

12 a target to enhance antitumor properties of curcumin.

13 g, showing stronger anti-cancer effects than curcumin.

14 that were assigned to the aromatic rings of curcumin.

15 tivation with IC50 only two-fold higher than curcumin.

16 i-inflammatory efficacy compared to standard curcumin.

17 s FOXP3 were upregulated in the colon by ETO-curcumin.

18 hen used as the wall material to encapsulate curcumin.

19 ncer cells and showed lower IC50 values than curcumin.

20 stases was associated with response to OXA + Curcumin.

21 d applications of metal complexes containing curcumin (=1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptad

22 ic resonance spectroscopy (NMR) as "deketene curcumin" (1,5-bis(4-hydroxy-3-methoxyphenyl)-1,4-pentad

23 parate cohort of mice was treated daily with curcumin, a clinically tested radioprotector, prior to a

24 Curcumin, a common ingredient of Asian spices, is known

25 and that SMSr oligomerization is promoted by curcumin, a drug known to perturb ER ceramide and calciu

26 Curcumin, a known antagonist of TNFalpha in multiple cel

27 ll culture conditions and during exposure to curcumin, a natural compound with anti-carcinogenic and

28 the exact targets and mechanism of action of curcumin, a natural product with anti-inflammatory and a

29 stance but was attenuated by the addition of Curcumin, a non-toxic NF-kappaB inhibitor.

30 Curcumin, a yellow-pigment compound found in the popular

31 Oxidative metabolites of curcumin adducted to and inhibited the inhibitor of NF-k

32 We found that curcumin administration increased miR-145 promoter activ

33 ohexanone (BM2) was 17 times more toxic than curcumin after 48 h incubation.

34 r experiments, liver cells were treated with curcumin after exposure to acrylamide.

35 We find that curcumin allows fibril-like structures containing the sa

36 ior protection from DSS-induced colitis than curcumin alone, highlighting the anti-inflammatory poten

37 STAT3 inhibition with micellar curcumin also suppressed postablation stimulation of dis

38 capacity of the liposomes was around 1.5% of curcumin, although the loading capacity of the hybrid mi

39 The spontaneous autoxidation distinguishes curcumin among natural polyphenolic compounds of therape

40 An unstable, alkynyl-tagged curcumin analog yielded abundant adducts with cellular p

41 Here, we characterize a novel curcumin analog, ASC-JM17, as an activator of central pa

42 Synthetic curcumin analogs that undergo oxidative transformation p

43 We have previously reported that curcumin analogs with a C7 linker bearing a C4-C5 olefin

44 lity, solubility and antioxidant activity of curcumin and additionally are biocompatible.

45 mers of Abeta42, which is stabilized both by curcumin and by Zn(2+.)

46 topology and geometry of interaction between curcumin and carrier.

47 In fact, the initial interaction between curcumin and CD-MOF is crucial for the formation of the

48 The interaction between curcumin and CD-MOFs is strong through hydrogen bond typ

49 least 3 orders of magnitude compared to free curcumin and curcumin:gamma-CD at pH 11.5.

50 active metabolites, increased the potency of curcumin and decreased the amount of curcumin-glutathion

51 Selective M-MDSC chemoresistence to curcumin and DTX was mediated by secretory/cytoplasmic c

52 dings suggest that the combined treatment of curcumin and essential turmeric oils provides superior p

53 rostaglandin E2 (PGE2) show that, esculetin, curcumin and hesperetin were the principal constituents

54 the suitability of the approach to stabilize curcumin and increase its bioaccessibility was assessed.

55 Curcumin and indigocarmine were selected as water insolu

56 In vivo, the combination of curcumin and IR had synergistic antitumor activity again

57 n this study, we demonstrate that, bioactive curcumin and its analog demethoxycurcumin are chiefly co

58 Curcumin and its analogs have been identified as potenti

59 v/v of methanol content) on the stability of curcumin and its analogues demethoxycurcumin and bisdeme

60 Curcumin and its chalcone derivatives inhibit the growth

61 ively as other anti-aging compounds, such as curcumin and metformin.

62 evaluation and design of clinical trials of curcumin and other polyphenols of medicinal interest.

63 ity for two extremely water insoluble drugs, curcumin and paclitaxel.

64 reviews the essential medicinal chemistry of curcumin and provides evidence that curcumin is an unsta

65 sed of resveratrol, ellagic acid, genistein, curcumin and quercetin to modulate biomarkers indicative

66 anti-aggregation effects of two polyphenols, curcumin and resveratrol, on the aggregation of islet am

67 on of two poorly soluble natural polyphenols curcumin and resveratrol.

68 one order of magnitude smaller than those of curcumin and resveratrol.

69 hobic interactions between aromatic rings of curcumin and the cavity of beta-cyclodextrin.

70 racellular co-release of the chemosensitizer curcumin and the encapsulated chemotherapeutic drug doxo

71 c agents, we compare the cellular effects of curcumin and the enone linker lead compound 1,7-bis(4-hy

72 , M1OH (which is one half of the molecule of curcumin) and dimer of dehydrozingerone, D1(OH)2, as ind

73 ve curcumin) to 146+/-3 degrees C (nanonized curcumin) and enthalpy from 27+/-2J/g to 3.5+/-1J/g.

74 examine the effect of vanillin, resveratrol, curcumin, and epigallocatechin-3-gallate (EGCG) on the a

75 es, such as n-3 polyunsaturated fatty acids, curcumin, and fermentable fiber, have been proposed to e

76 reconsolidate under the influence of dietary curcumin are impaired in an enduring manner; unlike exti

77 ide sequence, while those of resveratrol and curcumin are non-specific in that they stem from strong

78 Thus, identification of curcumin as a potential therapeutic for treating OM is o

79 Here, we identified curcumin as a pro-drug that requires oxidative activatio

80 Here, using [(14)C2]curcumin as a tracer, seven novel autoxidation products,

81 n of the bioavailability and bio-efficacy of curcumin as an amorphous solid dispersion (ASD) in a mat

82 ment and metastasis but might be targeted by curcumin as an antimetastatic strategy.

83 gative effect on the antioxidant activity of curcumin as assessed by the DPPH and ABTS assays.

84 hanced bio-efficacy compared to unformulated curcumin at 10-fold lower dose.

85 exhibited a lower degradation rate than free curcumin at 60 degrees C.

86 ed with the essential oil of C. longa L. and curcumin at a concentration of 0.5%.

87 Here, we examined the efficacy of dietary curcumin at impairing the consolidation and reconsolidat

88 vent in microextraction study to extract the curcumin at pH 4.0.

89 ils (ETO-curcumin) in comparison to standard curcumin at three specific doses (0, 5, 25 or 50 mg/kg),

90 icated to obtaining a small library of novel curcumin-based analogues, and a number of potent and bal

91 with 0.4, 4.0, and 40mug/ml nanoencapsulated curcumin before and after simulated gastric and intestin

92 Curcumin-beta-CD complex exhibited a sunlight stability

93 The application of curcumin-beta-CD complex in vanilla ice creams intensifi

94 Resveratrol and curcumin bind only to the hydrophobic residues near pept

95 Bovine serum albumin (BSA)/curcumin binding and dye photodegradation stability were

96 197 proteins were confidently identified as curcumin binding targets from HCT116 colon cancer cell l

97 y of lentivral-miR145 or orally administered curcumin blocked tumor progression in HNC-TICs in murine

98 soning and possibly many other activities of curcumin, but it is not known how many and what autoxida

99 11 selectively inhibited 5-LO, outperforming curcumin by a factor of up to 50, and impaired zymosan-i

100 erstanding the structural changes induced by curcumin can potentially lead to AD pharmaceutical agent

101 ed colorectal cancer survival in response to curcumin; combination of DCLK1-siRNA and curcumin dramat

102 by ABCG2 transporters with subtoxic doses of curcumin combined with stimulation of ATP hydrolysis by

103 Additionally, we proved that deketene curcumin, compared to curcumin, exhibits higher toxicity

104 BSA/curcumin complex showed 1:1 stoichiometry, but the therm

105 he thermal stability of Alg and Cur at algae/curcumin complex was 3.8% and 33% higher than their free

106 For the unfolded BSA/curcumin complex, it was found thatp DeltaH(o)F=-16.12kJ

107 leading to soluble and crystallizable metal curcumin complexes are outlined in detail.

108 PC-curcumin complexes were resistant to pepsin but were deg

109 and exciting medicinal applications of metal curcumin complexes, with the three most important areas

110 The curcumin concentration in enriched DES phase was analyze

111 ted safety in final results obtained for the curcumin concentration in the nanoparticles.

112 curcumin stability and water solubility but curcumin concentration inside the nanoparticles must be

113 A reliable method to determine the actual curcumin concentration must be validated since the valid

114 We found that curcumin conjugated with silica nanoparticles marginally

115 The curcumin-conjugated nanocapsules are found to be spheric

116 traordinarily amplified to more than 500% in curcumin-conjugated nanocapsules prepared from the above

117 mice via intramuscular (i.m.) injection, ELP-curcumin conjugates underwent a thermally triggered solu

118 ELP-curcumin conjugates were shown to display high drug load

119 oencapsulation structures increased with the curcumin content by incorporation of curcumin microcryst

120 lusion, we suggest that combination of OXA + Curcumin could be an effective treatment, for which CXCL

121 Curcumin (CUR) is a well-known natural compound, which e

122 Curcumin (Cur), a polyphenols with pharmacological funct

123 Curcumin degraded in emulsion under acid, alkali and UV

124 the experimental domain, half-life times of curcumin, demethoxycurcumin and bisdemethoxycurcumin wer

125 ethod for the analysis of main curcuminoids (curcumin, demethoxycurcumin and bisdemethoxycurcumin) pr

126 ne-3-one), formerly described as a synthetic curcumin derivative, were detected.

127 In this study, we show that curcumin, derived from Curcuma longa plant, long known f

128 The linear range of curcumin detection ranged from 1 to 100 mug/mL.

129 Inhibition of CSN5 by curcumin diminished cancer cell PD-L1 expression and sen

130 led nanoparticle formula of amphiphilic poly(curcumin-dithiodipropionic acid)-b-poly(ethylene glycol)

131 Functional validations confirmed that curcumin downregulates cellular protein synthesis, and i

132 to curcumin; combination of DCLK1-siRNA and curcumin dramatically reversed CSC phenotype, contributi

133 thout a STAT3 inhibitor (S3I-201 or micellar curcumin, eight arms).

134 videnced that non-polar microenvironment for curcumin embedded in nanogels was strengthened, which th

135 oscopy for the quantitative determination of curcumin encapsulated in poly(l-lactic acid) nanoparticl

136 The curcumin encapsulated NLC (CUR-NLC) was produced and opt

137 Furthermore, it was documented that curcumin enhanced the susceptibility of a marker strain

138 tested five candidate compounds: rifampicin, curcumin, epigallocatechin-3-gallate, myricetin, and scy

139 ts (l-ascorbic acid, caffeic acid, caffeine, curcumin, (-)-epigallocatechin gallate (EGCG), gallic ac

140 The encapsulated curcumin exhibited a lower degradation rate than free cu

141 Moreover, curcumin exhibited sustained release profile from crossl

142 e proved that deketene curcumin, compared to curcumin, exhibits higher toxicity on B78H1 melanoma cel

143 Sub-lethal curcumin exposure results in reduced bimodality of all h

144 LPS-activated RAW264.7 macrophages show that curcumin facilitates its anti-inflammatory action by ind

145 For native BSA/curcumin, fluorescence indicated an enthalpic and entrop

146 Fs, which can be used to store and stabilize curcumin for food applications.

147 hese results also justify the candidature of curcumin for the treatment of HPV18-infected cervical ca

148 tion, an anti-quorum sensing (anti-QS) agent curcumin from Curcuma longa (turmeric) was shown to inhi

149 d sweet pepper, piperine from ground pepper, curcumin from turmeric and curry, and myristicin from nu

150 s of magnitude compared to free curcumin and curcumin:gamma-CD at pH 11.5.

151 lts in formation of a unique complex between curcumin, gammaCD and potassium cations.

152 ency of curcumin and decreased the amount of curcumin-glutathione adducts in cells.

153 At optimal concentrations, curcumin greatly reduced expression levels of stem cell

154 regation is as follows: EGCG > resveratrol > curcumin > vanillin, consistent with experimental findin

155 Curcumin has anti-inflammatory and antioxidant effects a

156 Curcumin has been shown to have a wide variety of biolog

157 Addition of vitamin D and curcumin has been shown to increase the efficacy of IBD

158 linded, placebo controlled clinical trial of curcumin has been successful.

159 Curcumin has been successfully encapsulated in cyclodext

160 Curcumin has recently been classified as both a PAINS (p

161 e spice turmeric, with its active polyphenol curcumin, has been used as anti-inflammatory remedy in t

162 inogenic and anti-inflammatory properties of curcumin have been extensively investigated, identifying

163 Many cellular targets of curcumin have been identified, but how such a wide range

164 results suggest that less polar analogues of curcumin have potent cytotoxicity in vitro.

165 Other pro-inflammatory targets of curcumin (i.e., mPGES-1, cyclooxygenases, 12/15-LOs, nuc

166 Next, we show that dietary curcumin impairs the 'reconsolidation' of a recently for

167 However, ETO-curcumin improved disease activity index (DAI) dose-depe

168 s successful in retarding the degradation of curcumin in alkaline media (only 25-28 40% degraded in 1

169 All novel compounds were more effective than curcumin in apoptosis induction and cell cycle arrest at

170 e also made to enhance the solubilization of curcumin in aqueous equimolar mixed surfactant systems.

171 cating method could be employed to determine curcumin in bulk and emulsions.

172 ting HPLC-UV method for the determination of curcumin in Curcuma longa extract and emulsion was devel

173 was successfully applied to determination of curcumin in food and herbal tea samples.

174 MS with a simple dilution method to quantify curcumin in food condiments and dietary supplements.

175 GILZ was inducible by curcumin in macrophage cell lines, primary human monocyt

176 ion of the direct-binding protein targets of curcumin in situ.

177 owed distinctly better in vitro potency than curcumin in the four cancer cell lines.

178 Most importantly, the stability of curcumin in this complex was enhanced by at least 3 orde

179 The likely false activity of curcumin in vitro and in vivo has resulted in >120 clini

180 Spheroid cultures were disintegrated by curcumin in vitro but regrew within 30 to 40 days of tre

181 o display high drug loading, rapidly release curcumin in vitro via degradable carbamate bonds, and re

182 ion of the anti-inflammatory activity of ASD curcumin in vivo demonstrated enhanced bio-efficacy comp

183 tion containing essential turmeric oils (ETO-curcumin) in comparison to standard curcumin at three sp

184 In contrast, treatment of cells with curcumin increased the number of bleaching steps.

185 In fact, curcumin-induced up-regulation of SMAR1 ensures recruitm

186 We find that curcumin induces major structural changes in the Asp-23-

187 Pretreatment of the cells with curcumin inhibited radiation-induced NF-kappaBeta activi

188 pe and GILZ knock-out mice demonstrated that curcumin inhibits the activity of inflammatory regulator

189 eta40 differ only near the C-terminus, where curcumin interacts, while Zn(2+) interacts near the N-te

190 Curcumin is a constituent (up to approximately 5%) of th

191 Curcumin is a dietary anti-inflammatory and chemoprevent

192 Curcumin is a natural yellow-orange pigment extracted fr

193 Curcumin is a potent antioxidant agent having versatile

194 Curcumin is a potent substance with several functions, i

195 Additional experiments revealed that dietary curcumin is also effective at impairing the reconsolidat

196 istry of curcumin and provides evidence that curcumin is an unstable, reactive, nonbioavailable compo

197 findings indicate that a diet enriched with curcumin is capable of impairing fear memory consolidati

198 In conclusion, deketene curcumin is formed as a consequence of pyrolysis during

199 e degradation study proves that stability of curcumin is improved dramatically in such nanocapsules d

200 Curcumin is known to induce apoptosis of cancer cells by

201 Curcumin is known to trigger ER-stress induced cell deat

202 A mechanism for the autoxidation of curcumin is proposed that accounts for the addition and

203 In each case, the use of curcumin is shown to promote analyte ionization very eff

204 Curcumin is the major active ingredient of turmeric and

205 Although curcumin is the most studied active constituents of turm

206 Curcumin is unstable at physiological pH and rapidly deg

207 Curcumin is widely used in traditional Asian kitchen as

208 A number of more hydrophilic curcumin isoforms and decomposition products, including

209 e (nFTP) technology and investigated whether curcumin leads to intracellular AD pathologic changes.

210 We first demonstrated that curcumin, like docetaxel (DTX), can selectively target C

211 ative to analogs with the original di-ketone curcumin linker was apparent.

212 Interestingly, dissolving the curcumin loaded CD-MOFs crystals in water results in for

213 biocompatibility (using calf-thymus DNA) of curcumin-loaded mixed surfactant formulations were also

214 ty Pathway Analysis(TM) (IPA) suggested that curcumin may exert its anticancer effects over multiple

215 cumin remained constant, suggesting that ETO-curcumin may provide superior anti-inflammatory efficacy

216 ith the curcumin content by incorporation of curcumin microcrystals upon electrospraying.

217 -pentadien-3-ones were designed as potential curcumin mimics, structurally featuring a central five-c

218 report a poly(lactic-co-glycolic acid) based curcumin nanoparticle formulation (Nano-CUR).

219 The millet protein-curcumin nanoparticles were spherical with diameter arou

220 Bioactivation of curcumin occurred readily in vitro, which may explain th

221 We measure the effects of Zn(2+) and curcumin on Abeta40, and compare these with their previo

222 ad greater growth inhibitory activities than curcumin on APL cells.

223 However, the effects of curcumin on intracellular AD pathologic processes remain

224 The antibiofilm potential of curcumin on uropathogens as well as its efficacy in dist

225 The current study examines effect of curcumin on: 1) systemic T helper 17 (Th17) cell respons

226 ein that were decreased by pretreatment with curcumin or an unstable analog but not by a stable analo

227 of the antiepileptic efficacy (for example, curcumin) or antiepileptogenic affect (for example, ator

228 o in situ formation of a depot that released curcumin over 4days post-injection and decreased plasma

229 The concomitant combination of Curcumin + OXA was more effective and synergistic in cel

230 ximately 15mN/m in the presence of amorphous curcumin particles in water phase compared to crystallin

231 After nanonization, native crystalline curcumin particles were converted into amorphous, nanosi

232 In this study, nano-sized amorphous curcumin particles were fabricated using nanonization te

233 icles in water phase compared to crystalline curcumin particles.

234 BSA (mainly native) increased the curcumin photodegradation stability.

235 However, the poor oral bioavailability of curcumin poses a significant pharmacological barrier to

236 d gene expression alterations of a specific, curcumin preparation containing essential turmeric oils

237 We show that a diet enriched with 1.5% curcumin prevents the training-related elevation in the

238 ed when tumor-bearing mice were treated with curcumin prior to IR.

239 Here we synthesized a cell permeable curcumin probe (Cur-P) with an alkyne moiety, which can

240 r the effects of herbs (such as cannabis and curcumin), probiotics, acupuncture, exercise, and mind-b

241 Here, we report that curcumin promotes the survival of DCLK1-positive colon C

242 Thus ASD curcumin provides a more potent and efficacious formulat

243 tment with the breast CSC-targeting compound curcumin rapidly extinguished McTN in breast CSC, preven

244 minoids have a different mode of action than curcumin, rapidly and specifically depleting thiol level

245 revealed that exposure to AS-HK014, but not curcumin, rapidly depleted glutathione and trypanothione

246 tiple-ring compounds, EGCG, resveratrol, and curcumin, redirect Abeta(17-36) from a fibrillar aggrega

247 In summary, curcumin reduced soluble Tau and elevated HSPs involved

248 rmacological inhibition of JNK (SP600125) or curcumin reduced transcriptional up-regulation of acid c

249 The results indicate that curcumin reduces the effects of reactive oxygen species

250 e the anti-inflammatory efficacy of standard curcumin remained constant, suggesting that ETO-curcumin

251 Intriguingly, curcumin remarkably reduced the level of intracellular o

252 Thus, our results provided evidence that curcumin's mechanism of action in attenuating AD patholo

253 In CRANAD-17, a curcumin scaffold was used as an anchoring moiety to ush

254 Curcumin seems to be a promising host modulatory agent i

255 Curcumin selectively suppressed levels of soluble Tau di

256 e inconclusive results in human studies with curcumin so far.

257 ed the AL-type which confirms an increase in curcumin solubility by increasing the concentration of b

258 physicochemical properties of self-assembled curcumin-soluble soybean polysaccharide (SSPS) nanoparti

259 ely 90% were self-assembled after increasing curcumin-SSPS mixture to pH 12.0 and lowering pH to 7.0.

260 lymers is a promising alternative to improve curcumin stability and water solubility but curcumin con

261 Curcumin stabilized O/W emulsion has an initial droplet

262 es of the essential oil of the plant and the curcumin standard interfered with mycotoxin production.

263 Curcumin suppressed CXCL5 expression by direct inhibitio

264 A synthetic monoketone analog of curcumin, termed 3, 5-bis (2-flurobenzylidene) piperidin

265 e investigated the solubility enhancement of curcumin through inclusion complexation by beta-cyclodex

266 The binding of curcumin to native-like phosphocaseins (PC) dispersed in

267 (p=0.05) increase in the binding constant of curcumin to processed PC, which may result from the sign

268 MPa did not affect the binding parameters of curcumin to processed PC.

269 table depot for sustained, local delivery of curcumin to treat neuroinflammation.

270 melting point from 177+/-1 degrees C (native curcumin) to 146+/-3 degrees C (nanonized curcumin) and

271 Curcumin-treated mice showed significant decreases in bo

272 more efficiently down-regulated after OXA + Curcumin treatment as compared to the sensitive cells.

273 Our results suggest that curcumin treatment induces HuR expression.

274 Curcumin treatment polarized surviving M-MDSCs toward CC

275 hippocampus was reduced further (83%-81%) by curcumin treatment.

276 riodontitis; 2) group 2 = periodontitis with curcumin treatment; 3) group 3 = periodontally healthy w

277 ent; 3) group 3 = periodontally healthy with curcumin treatment; and 4) group 4 = periodontally healt

278 sent study showed that both ETO and standard curcumin treatments provided protection against DSS-indu

279 However, curcumin unexpectedly induced proliferation and autophag

280 ethod for separation and preconcentration of curcumin using deep eutectic solvent known as green solv

281 in, umbelliferone, esculetin, hesperetin and curcumin, using the orthogonal design, uniform design an

282 Curcumin was administered via oral gavage (30 mg/kg/d) f

283 The treatment with curcumin was also found to attenuate the QS-dependent fa

284 rmacokinetic studies in rats showed that ASD curcumin was approximately 13-fold more bioavailable com

285 For this purpose, the phase solubility of curcumin was assessed using Higuchi and Connors method,

286 Curcumin was complexed with beta-CD using co-precipitati

287 dynamic and static quenching mechanisms and curcumin was distributed in a palisade layer of mixed ag

288 In our study, curcumin was identified as a lead compound for the simul

289 lity to solubilize a model hydrophobic drug, curcumin, was also explored.

290 The intra-day precision and accuracy for curcumin were 0.87% and 2.0%, while the inter-day precis

291 EGCG, gallic acid, and curcumin were identified as a multifunctional compounds,

292 acid, base, oxidation, heat and UV light) of curcumin were performed in emulsion.

293 6-bis benzylidine cyclohexanone analogues of curcumin were synthesized, and their inhibitory effects

294 a more potent and efficacious formulation of curcumin which may also help in masking the colour, tast

295 present work focuses on the natural product curcumin, which has previously been reported to inhibit

296 Replacing the heptadienedione moiety of curcumin with a monocarbonyl cross-conjugated dienone em

297 To evaluate this, we pyrolysed curcumin with and without coconut fat or olive oil, and

298 eported that replacement of two OH groups in curcumin with less polar groups like methoxy increases i

299 redict the binding position and mechanism of curcumin with self-assemblies.

300 Microencapsulation of curcumin within the proposed hybrid structures significa