Vanillin Improves and Prevents Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice

Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-me...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of pharmacology and experimental therapeutics Vol. 330; no. 2; pp. 370 - 376
Main Authors Wu, Shih-Lu, Chen, Jaw-Chyun, Li, Chia-Cheng, Lo, Hsin-Yi, Ho, Tin-Yun, Hsiang, Chien-Yun
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.08.2009
American Society for Pharmacology and Experimental Therapeutics
Subjects
Online AccessGet full text

Cover

Loading…
Abstract Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-κB (NF-κB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-κB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-κB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-κB(IκB)-α phosphorylation, and IκB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.
AbstractList Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-kappaB (NF-kappaB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-kappaB (NF-kappaB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-kappaB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-kappaB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-kappaB(IkappaB)-alpha phosphorylation, and IkappaB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1beta, IL-6, interferon-gamma, and tumor necrosis factor-alpha] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.
Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-κB (NF-κB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-κB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-κB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-κB(IκB)-α phosphorylation, and IκB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.
Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-κB (NF-κB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-κB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-κB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-κB(IκB)-α phosphorylation, and IκB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1β, IL-6, interferon-γ, and tumor necrosis factor-α] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.
Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-kappaB (NF-kappaB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-kappaB (NF-kappaB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-kappaB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-kappaB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-kappaB(IkappaB)-alpha phosphorylation, and IkappaB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1beta, IL-6, interferon-gamma, and tumor necrosis factor-alpha] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-kappaB (NF-kappaB) and production of proinflammatory cytokines play important roles in the pathogenesis of IBD. In this study, the effect of vanillin (4-hydroxy-3-methoxybenzaldehyde), a potent nuclear factor-kappaB (NF-kappaB) inhibitor, was evaluated in mice with trinitrobenzene sulfonic acid (TNBS)-induced colitis. Oral administration of vanillin improved macroscopic and histological features of TNBS-induced colitis in a dose-dependent manner. Vanillin not only prevented TNBS-induced colitis but also ameliorated the established colitis. By in vivo NF-kappaB bioluminescence imaging, electrophoretic mobility shift assay, and Western blot, we found that vanillin suppressed in vivo NF-kappaB activities through the inhibition of p65 translocation, inhibitor of nuclear factor-kappaB(IkappaB)-alpha phosphorylation, and IkappaB kinase activation. Furthermore, vanillin reduced the expressions of proinflammatory cytokines [interleukin (IL)-1beta, IL-6, interferon-gamma, and tumor necrosis factor-alpha] and stimulated the expression of anti-inflammatory cytokine (IL-4) in colonic tissues. In conclusion, this work identified vanillin as an anti-inflammatory compound with the capacity to prevent and ameliorate TNBS-induced colitis. Due to its safety, vanillin could be a potent candidate for the treatment of IBD.
Author Lo, Hsin-Yi
Chen, Jaw-Chyun
Ho, Tin-Yun
Hsiang, Chien-Yun
Wu, Shih-Lu
Li, Chia-Cheng
Author_xml – sequence: 1
  givenname: Shih-Lu
  surname: Wu
  fullname: Wu, Shih-Lu
– sequence: 2
  givenname: Jaw-Chyun
  surname: Chen
  fullname: Chen, Jaw-Chyun
– sequence: 3
  givenname: Chia-Cheng
  surname: Li
  fullname: Li, Chia-Cheng
– sequence: 4
  givenname: Hsin-Yi
  surname: Lo
  fullname: Lo, Hsin-Yi
– sequence: 5
  givenname: Tin-Yun
  surname: Ho
  fullname: Ho, Tin-Yun
– sequence: 6
  givenname: Chien-Yun
  surname: Hsiang
  fullname: Hsiang, Chien-Yun
  email: cyhsiang@mail.cmu.edu.tw
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19423842$$D View this record in MEDLINE/PubMed
BookMark eNp9kE1r3DAQhkVJaDZpz70Vn3rzRh-WbR3D0jQLKS1kk6uQ5XF2gi1tJXlL-uursFsChfY0M_C8M8NzTk6cd0DIB0aXjPHq8mkHacmoWjLJWyHfkEVuWEkZFSdkQSnnpZC1PCPnMT5RyqqqFm_JGVMVF23FF2TzYByOI7piPe2C30MsjOuL7wH24FIsNgEdpuA7cL_AQXE3j4N3aIsri325dv1soS9WfsSEschrvqKFd-R0MGOE98d6Qe6vP29WN-Xtty_r1dVtaUVTp5JXHR-ajlvbtoOyjZF91dKBGckrI5qGtaB6pRoFfdPJeqCiZjUX3UBZa6VS4oJ8OuzNn_-YISY9YbQwjsaBn6OuG8lYRVkGPx7BuZug17uAkwnP-o-HDFweABt8jAGGV4TqF9P6xXQelD6Yzgn5V8JiMgm9S8Hg-J_c8ectPm5_YgC925owGetH__ishaCaa9HQDKoDCNngHiHoaBFc1p1DNune4z-P_AbszqLt
CitedBy_id crossref_primary_10_1186_s12917_015_0410_0
crossref_primary_10_1016_j_toxrep_2015_11_001
crossref_primary_10_2174_1389557519666190312164355
crossref_primary_10_1155_2014_942196
crossref_primary_10_1021_acs_jafc_6b05697
crossref_primary_10_1155_2019_2129350
crossref_primary_10_18632_oncotarget_14758
crossref_primary_10_1016_j_bbagen_2010_11_004
crossref_primary_10_1016_j_fct_2012_02_025
crossref_primary_10_1016_j_intimp_2011_12_014
crossref_primary_10_1089_ten_tea_2012_0001
crossref_primary_10_4028_www_scientific_net_AMR_230_232_857
crossref_primary_10_1080_14786419_2020_1753056
crossref_primary_10_4028_www_scientific_net_AMR_230_232_935
crossref_primary_10_3109_13880209_2013_799707
crossref_primary_10_1039_D4SU00488D
crossref_primary_10_1271_bbb_110700
crossref_primary_10_1371_journal_pone_0031808
crossref_primary_10_1016_j_ejmcr_2022_100055
crossref_primary_10_4028_www_scientific_net_KEM_480_481_484
crossref_primary_10_1016_j_ijbiomac_2018_10_053
crossref_primary_10_3892_mmr_2018_8401
crossref_primary_10_3390_toxins5122353
crossref_primary_10_3892_etm_2019_7242
crossref_primary_10_1016_j_foodchem_2012_07_124
crossref_primary_10_3233_RNN_201028
crossref_primary_10_1016_j_biopha_2019_109196
crossref_primary_10_1371_journal_pone_0034969
crossref_primary_10_1039_C8RA03626H
crossref_primary_10_1016_j_scp_2021_100471
crossref_primary_10_4155_fmc_2018_0432
crossref_primary_10_1016_j_ejphar_2023_176153
crossref_primary_10_1016_j_jep_2010_08_013
crossref_primary_10_1186_s40543_014_0021_6
crossref_primary_10_1155_2018_6231482
crossref_primary_10_4028_www_scientific_net_KEM_480_481_250
crossref_primary_10_1016_j_rechem_2022_100453
crossref_primary_10_4028_www_scientific_net_KEM_480_481_496
crossref_primary_10_5483_BMBRep_2012_45_5_265
crossref_primary_10_1097_NT_0000000000000412
crossref_primary_10_1016_j_indcrop_2015_05_037
crossref_primary_10_1039_C6FO01770C
crossref_primary_10_3390_ijms18020389
crossref_primary_10_1021_acs_jafc_8b01582
crossref_primary_10_3390_nutraceuticals4040030
crossref_primary_10_1016_j_fct_2012_05_054
crossref_primary_10_1155_2015_626028
crossref_primary_10_1517_17425247_2014_891581
crossref_primary_10_1177_0960327119831067
crossref_primary_10_1016_j_nano_2015_07_003
crossref_primary_10_1021_bm400256h
crossref_primary_10_1039_c3ra46396f
crossref_primary_10_1271_bbb_110524
crossref_primary_10_3390_molecules171113622
crossref_primary_10_1016_j_bioorg_2019_103057
crossref_primary_10_1152_physrev_00040_2012
crossref_primary_10_1016_j_sciaf_2022_e01506
crossref_primary_10_1016_j_trsl_2016_04_009
crossref_primary_10_1021_acs_jafc_7b04259
crossref_primary_10_1089_jmf_2012_0162
crossref_primary_10_3390_molecules23123283
crossref_primary_10_1002_iid3_1366
crossref_primary_10_3390_antiox13121544
crossref_primary_10_1016_j_pbb_2014_03_022
crossref_primary_10_3389_fphar_2018_01511
Cites_doi 10.1016/S0015-6264(67)82961-4
10.1023/A:1007048313556
10.1016/j.mrfmmm.2004.02.024
10.1172/JCI119823
10.1111/j.1365-2672.2004.02275.x
10.1152/ajpgi.1990.258.4.G527
10.1016/S0016-5085(00)70007-2
10.1038/nm0996-998
10.1038/nri2340
10.1016/S0031-9422(03)00149-3
10.1016/j.ejps.2005.01.015
10.1002/em.2860080803
10.1006/abio.1976.9999
10.1136/gut.42.4.477
10.1111/j.1572-0241.2000.03360.x
10.1142/S0192415X0800651X
10.1056/NEJM199704103361506
10.4049/jimmunol.168.3.1441
10.1002/ibd.20352
10.1146/annurev.immunol.20.100301.064816
10.4049/jimmunol.157.5.2174
10.1016/j.biomaterials.2007.07.005
10.1142/S0192415X08006235
10.1084/jem.182.5.1281
10.1080/10715760500177880
10.1016/j.bcp.2005.03.008
10.1016/0003-9861(92)90433-W
10.1111/j.1365-2249.1993.tb05997.x
10.1016/S0953-6205(00)00090-X
10.1016/0165-7992(87)90033-9
10.1002/eji.1830270722
10.1203/PDR.0b013e318163a897
10.1016/0304-3835(95)03833-I
10.1146/annurev.immunol.18.1.621
10.1021/jf030319d
10.1002/path.1409
10.1124/mol.108.049502
10.1016/0015-6264(77)90086-4
ContentType Journal Article
Copyright 2009 American Society for Pharmacology and Experimental Therapeutics
Copyright_xml – notice: 2009 American Society for Pharmacology and Experimental Therapeutics
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1124/jpet.109.152835
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList MEDLINE


MEDLINE - Academic
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Pharmacy, Therapeutics, & Pharmacology
EISSN 1521-0103
EndPage 376
ExternalDocumentID 19423842
10_1124_jpet_109_152835
330_2_370
S0022356524385416
Genre Research Support, Non-U.S. Gov't
Journal Article
Comparative Study
GroupedDBID ---
-~X
.55
.GJ
0R~
18M
2WC
3O-
4.4
53G
5GY
5RE
5VS
8WZ
A6W
AALRI
AAXUO
AAYOK
ABCQX
ABIVO
ABJNI
ABOCM
ABSQV
ACGFO
ACGFS
ACNCT
ADBBV
ADCOW
ADIYS
AENEX
AERNN
AETEA
AFFNX
AFOSN
AGFXO
AI.
ALMA_UNASSIGNED_HOLDINGS
BAWUL
BTFSW
CS3
DIK
DU5
E3Z
EBS
EJD
F5P
F9R
FDB
GX1
H13
HZ~
INIJC
KQ8
L7B
LSO
M41
MJL
MVM
O9-
OHT
P2P
R.V
R0Z
RHI
ROL
RPT
TR2
UQL
VH1
W8F
WH7
WOQ
X7M
YBU
YHG
YQT
ZGI
ZXP
-
0R
55
8RP
AALRV
ABFLS
ABSGY
ABZEH
ACDCL
ADACO
ADBIT
ADKFC
AIKQT
DL
FH7
HZ
O0-
OK1
RHF
W2D
X
AAYXX
ACVFH
ADCNI
AEUPX
AFPUW
AIGII
AKBMS
AKYEP
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
ID FETCH-LOGICAL-c376t-24b2f7b2cc88f9c7a5d480f1a524a37718e9d9979ed7b56f0361623bf018c5993
ISSN 0022-3565
1521-0103
IngestDate Fri Jul 11 00:32:14 EDT 2025
Sat Mar 08 01:25:20 EST 2025
Tue Jul 01 05:28:57 EDT 2025
Thu Apr 24 23:08:36 EDT 2025
Tue Jan 05 21:16:54 EST 2021
Sat Mar 08 15:43:27 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 2
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c376t-24b2f7b2cc88f9c7a5d480f1a524a37718e9d9979ed7b56f0361623bf018c5993
Notes ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
PMID 19423842
PQID 67511401
PQPubID 23479
PageCount 7
ParticipantIDs proquest_miscellaneous_67511401
pubmed_primary_19423842
crossref_primary_10_1124_jpet_109_152835
crossref_citationtrail_10_1124_jpet_109_152835
highwire_pharmacology_330_2_370
elsevier_sciencedirect_doi_10_1124_jpet_109_152835
ProviderPackageCode RHF
RHI
CITATION
AAYXX
PublicationCentury 2000
PublicationDate August 2009
20090801
2009-08-00
2009-Aug
PublicationDateYYYYMMDD 2009-08-01
PublicationDate_xml – month: 08
  year: 2009
  text: August 2009
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle The Journal of pharmacology and experimental therapeutics
PublicationTitleAlternate J Pharmacol Exp Ther
PublicationYear 2009
Publisher Elsevier Inc
American Society for Pharmacology and Experimental Therapeutics
Publisher_xml – name: Elsevier Inc
– name: American Society for Pharmacology and Experimental Therapeutics
References Lee CH, Wu SL, Chen JC, Li CC, Lo HY, Cheng WY, Lin JG, Chang YH, Hsiang CY, and Ho TY (2008)
2766-2776.
Strober W, Fuss IJ, and Blumberg RS (2002) The immunology of mucosal models of inflammation.
1603-1611.
Kirwin CJ and Galvin JB (1993) Ethers, in
Opdyke DLJ (1977) Fragrance raw materials monographs. Vanillin.
Karin M and Ben-Neriah Y (2000) Phosphorylation meets ubiquitination: the control of NF-κB activity.
metastasis of mouse breast cancer cells.
1743-1750.
Cho JH (2008) The genetics and immunopathogenesis of inflammatory bowel disease.
Economou M and Pappas G (2008) New global map of Crohn’s disease: genetic, environmental, and socioeconomic correlations.
709-720.
Akagi K, Hirose M, Hoshiya T, Mizoguchi Y, Ito N, and Shirai T (1995) Modulating effects of ellagic acid, vanillin and quercetin in a rat medium term multi-organ carcinogenesis model.
Ho TY, Chen YS, and Hsiang CY (2007) Noninvasive nuclear factor-κB bioluminescence imaging for the assessment of host-biomaterial interaction in transgenic mice.
Kamat JP, Ghosh A, and Devasagayam TP (2000) Vanillin as an antioxidant in rat liver mitochondria: inhibition of protein oxidation and lipid peroxidation induced by photosensitization.
57-65.
Jansson T and Zech L (1987) Effects of vanillin on sister-chromatid exchanges and chromosome aberrations in human lymphocytes.
446-451.
Neurath MF, Pettersson S, Meyer zum Büschenfelde KH, and Strober W (1996) Local administration of antisense phosphorothioate oligonucleotides to the p65 subunit of NF-κB abrogates established experimental colitis in mice.
4370-4377.
(Clayton GD and Clayton FE eds) pp 445-525, John Wiley & Sons, New York.
191-196.
Hagan EC, Hansen WH, Fitzhugh OG, Jenner PM, Jones WI, Taylor JM, Long EL, Nelson AA, and Brouwer JB (1967) Food flavourings and compounds of related structure. II. Subacute and chronic toxicity.
Hogaboam CM, Vallance BA, Kumar A, Addison CL, Graham FL, Gauldie J, and Collins SM (1997) Therapeutic effects of interleukin-4 gene transfer in experimental inflammatory bowel disease.
Holland N, Dong J, Garnett E, Shaikh N, Huen K, Harmatz P, Olive A, Winter HS, Gold BD, Cohen SA, et al. (2008) Reduced intracellular T-helper 1 interferon-γ in blood of newly diagnosed children with Crohn’s disease and age-related changes in Th1/Th2 cytokine profiles.
3452-3457.
Bradford MM (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding.
2174-2185.
477-484.
221-224.
1185-1198.
Fitzgerald DJ, Stratford M, Gasson MJ, Ueckert J, Bos A, and Narbad A (2004) Mode of antimicrobial action of vanillin against
Lirdprapamongkol K, Sakurai H, Kawasaki N, Choo MK, Saitoh Y, Aozuka Y, Singhirunnusorn P, Ruchirawat S, Svasti J, and Saiki I (2005) Vanillin suppresses
113-121.
1163-1172.
Kruidenier L, Kuiper I, Lamers CB, and Verspaget HW (2003) Intestinal oxidative damage in inflammatory bowel disease: semi-quantification, localization, and association with mucosal antioxidants.
mutagenicity tests. II. Results from the testing of 270 chemicals.
633-638.
104-113.
Sands BE (2000) Therapy of inflammatory bowel disease.
Wallace JL and Keenan CM (1990) An orally active inhibitor of leukotriene synthesis accelerates healing in a rat model of colitis.
257-262.
151-157.
1281-1290.
Walton NJ, Mayer MJ, and Narbad A (2003) Vanillin.
559-566.
Schreiber S, Nikolaus S, and Hampe J (1998) Activation of nuclear factor-κBin inflammatory bowel disease.
621-663.
495-549.
and
leaf and its triterpenes inhibited lipopolysaccharide-induced cytokines and inducible enzyme production via the nuclear factor-κB signaling pathway in lung epithelial cells.
28-36.
Russel MG (2000) Changes in the incidence of inflammatory bowel disease: what does it mean?
Mortelmans K, Haworth S, Lawlor T, Speck W, Tainer B, and Zeiger E (1986)
Ischiropoulos H, Zhu L, and Beckman JS (1992) Peroxynitrite formation from macrophage-derived nitric oxide.
47-53.
1066-1071.
Carlsen H, Moskaug JØ, Fromm SH, and Blomhoff R (2002) In vivo imaging of NF-κB activity.
Cheng WY, Wu SL, Hsiang CY, Li CC, Lai TY, Lo HY, Shen WS, Lee CH, Chen JC, Wu HC, et al. (2008) Relationship between San-Huang-Xie-Xin-Tang and its herbal components on the gene expression profiles in HepG2 cells.
tetradecanoylphorbol-13-acetate-induced hepatocellular transformation via activator protein 1 signaling pathway and cell cycle progression.
G527-G534.
1441-1446.
505-515.
Barnes PJ and Karin M (1997) Nuclear factor-κB: a pivotal transcription factor in chronic inflammatory diseases.
Bantel H, Berg C, Vieth M, Stolte M, Kruis W, and Schulze-Osthoff K (2000) Mesalazine inhibits activation of transcription factor NF-κB in inflamed mucosa of patients with ulcerative colitis.
Hanauer SB and Meyers S (1997) Management of Crohn’s disease in adults.
Carlsen H, Alexander G, Austenaa LM, Ebihara K, and Blomhoff R (2004) Molecular imaging of the transcription factor NF-κB, a primary regulator of stress response.
199-211.
248-254.
Hsiang CY, Wu SL, and Ho TY (2005) Morin inhibited 12-
783-797.
Elson CO, Beagley KW, Sharmanov AT, Fujihashi K, Kiyono H, Tennyson GS, Cong Y, Black CA, Ridwan BW, and McGhee JR (1996) Hapten-induced model of murine inflammatory bowel disease: mucosa immune responses and protection by tolerance.
Reinecker HC, Steffen M, Witthoeft T, Pflueger I, Schreiber S, MacDermott RP, and Raedler A (1993) Enhanced secretion of tumour necrosis factor-α, IL-6, and IL-1β by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn’s disease.
Neurath MF, Fuss I, Pasparakis M, Alexopoulou L, Haralambous S, Meyer zum Büschenfelde KH, Strober W, and Kollias G (1997) Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice.
Liang JA, Wu SL, Lo HY, Hsiang CY, and Ho TY (2009) Vanillin inhibits matrix metalloproteinase-9 expression through down-regulation of nuclear factor-κB signaling pathway in human hepatocellular carcinoma cells.
Neurath MF, Fuss I, Kelsall BL, Stüber E, and Strober W (1995) Antibodies to interleukin 12 abrogate established experimental colitis in mice.
141-157.
Murakami Y, Hirata A, Ito S, Shoji M, Tanaka S, Yasui T, Machino M, and Fujisawa S (2007) Re-evaluation of cyclooxygenase-2-inhibiting activity of vanillin and guaiacol in macrophages stimulated with lipopolysaccharide.
458-466.
Joshi R, Kumar S, Unnikrishnan M, and Mukherjee T (2005) Free radical scavenging reactions of sulfasalazine, 5-aminosalicylic acid and sulfapyridine: mechanistic aspects and antioxidant activity.
998-1004.
invasion and
S68-S82.
Santosh Kumar SS, Priyadarsini KI, and Sainis KB (2004) Inhibition of peroxynitrite-mediated reactions by vanillin.
801-807.
174-181.
139-145.
1-119.
10.1124/jpet.109.152835_bib8
10.1124/jpet.109.152835_bib7
10.1124/jpet.109.152835_bib9
10.1124/jpet.109.152835_bib18
10.1124/jpet.109.152835_bib19
10.1124/jpet.109.152835_bib16
10.1124/jpet.109.152835_bib38
10.1124/jpet.109.152835_bib17
10.1124/jpet.109.152835_bib39
10.1124/jpet.109.152835_bib14
10.1124/jpet.109.152835_bib36
10.1124/jpet.109.152835_bib15
10.1124/jpet.109.152835_bib37
10.1124/jpet.109.152835_bib12
10.1124/jpet.109.152835_bib34
10.1124/jpet.109.152835_bib13
10.1124/jpet.109.152835_bib35
10.1124/jpet.109.152835_bib10
10.1124/jpet.109.152835_bib32
10.1124/jpet.109.152835_bib11
10.1124/jpet.109.152835_bib33
10.1124/jpet.109.152835_bib30
10.1124/jpet.109.152835_bib31
10.1124/jpet.109.152835_bib29
10.1124/jpet.109.152835_bib27
10.1124/jpet.109.152835_bib28
10.1124/jpet.109.152835_bib25
10.1124/jpet.109.152835_bib26
10.1124/jpet.109.152835_bib23
10.1124/jpet.109.152835_bib24
10.1124/jpet.109.152835_bib4
10.1124/jpet.109.152835_bib21
10.1124/jpet.109.152835_bib3
10.1124/jpet.109.152835_bib22
10.1124/jpet.109.152835_bib6
10.1124/jpet.109.152835_bib41
10.1124/jpet.109.152835_bib5
10.1124/jpet.109.152835_bib20
10.1124/jpet.109.152835_bib40
10.1124/jpet.109.152835_bib2
10.1124/jpet.109.152835_bib1
References_xml – reference: Murakami Y, Hirata A, Ito S, Shoji M, Tanaka S, Yasui T, Machino M, and Fujisawa S (2007) Re-evaluation of cyclooxygenase-2-inhibiting activity of vanillin and guaiacol in macrophages stimulated with lipopolysaccharide.
– reference: Opdyke DLJ (1977) Fragrance raw materials monographs. Vanillin.
– reference: Fitzgerald DJ, Stratford M, Gasson MJ, Ueckert J, Bos A, and Narbad A (2004) Mode of antimicrobial action of vanillin against
– reference: and
– reference: 2174-2185.
– reference: 1743-1750.
– reference: Hogaboam CM, Vallance BA, Kumar A, Addison CL, Graham FL, Gauldie J, and Collins SM (1997) Therapeutic effects of interleukin-4 gene transfer in experimental inflammatory bowel disease.
– reference: Karin M and Ben-Neriah Y (2000) Phosphorylation meets ubiquitination: the control of NF-κB activity.
– reference: Sands BE (2000) Therapy of inflammatory bowel disease.
– reference: 458-466.
– reference: Neurath MF, Fuss I, Kelsall BL, Stüber E, and Strober W (1995) Antibodies to interleukin 12 abrogate established experimental colitis in mice.
– reference: 709-720.
– reference: 248-254.
– reference: 446-451.
– reference: Cheng WY, Wu SL, Hsiang CY, Li CC, Lai TY, Lo HY, Shen WS, Lee CH, Chen JC, Wu HC, et al. (2008) Relationship between San-Huang-Xie-Xin-Tang and its herbal components on the gene expression profiles in HepG2 cells.
– reference: 1163-1172.
– reference: 141-157.
– reference: leaf and its triterpenes inhibited lipopolysaccharide-induced cytokines and inducible enzyme production via the nuclear factor-κB signaling pathway in lung epithelial cells.
– reference: Jansson T and Zech L (1987) Effects of vanillin on sister-chromatid exchanges and chromosome aberrations in human lymphocytes.
– reference: Lirdprapamongkol K, Sakurai H, Kawasaki N, Choo MK, Saitoh Y, Aozuka Y, Singhirunnusorn P, Ruchirawat S, Svasti J, and Saiki I (2005) Vanillin suppresses
– reference: Russel MG (2000) Changes in the incidence of inflammatory bowel disease: what does it mean?
– reference: 1281-1290.
– reference: G527-G534.
– reference: Walton NJ, Mayer MJ, and Narbad A (2003) Vanillin.
– reference: Hanauer SB and Meyers S (1997) Management of Crohn’s disease in adults.
– reference: 191-196.
– reference: mutagenicity tests. II. Results from the testing of 270 chemicals.
– reference: 4370-4377.
– reference: 1-119.
– reference: 57-65.
– reference: Carlsen H, Alexander G, Austenaa LM, Ebihara K, and Blomhoff R (2004) Molecular imaging of the transcription factor NF-κB, a primary regulator of stress response.
– reference: Barnes PJ and Karin M (1997) Nuclear factor-κB: a pivotal transcription factor in chronic inflammatory diseases.
– reference: -tetradecanoylphorbol-13-acetate-induced hepatocellular transformation via activator protein 1 signaling pathway and cell cycle progression.
– reference: 113-121.
– reference: Kruidenier L, Kuiper I, Lamers CB, and Verspaget HW (2003) Intestinal oxidative damage in inflammatory bowel disease: semi-quantification, localization, and association with mucosal antioxidants.
– reference: metastasis of mouse breast cancer cells.
– reference: Bantel H, Berg C, Vieth M, Stolte M, Kruis W, and Schulze-Osthoff K (2000) Mesalazine inhibits activation of transcription factor NF-κB in inflamed mucosa of patients with ulcerative colitis.
– reference: 47-53.
– reference: Liang JA, Wu SL, Lo HY, Hsiang CY, and Ho TY (2009) Vanillin inhibits matrix metalloproteinase-9 expression through down-regulation of nuclear factor-κB signaling pathway in human hepatocellular carcinoma cells.
– reference: 633-638.
– reference: Elson CO, Beagley KW, Sharmanov AT, Fujihashi K, Kiyono H, Tennyson GS, Cong Y, Black CA, Ridwan BW, and McGhee JR (1996) Hapten-induced model of murine inflammatory bowel disease: mucosa immune responses and protection by tolerance.
– reference: 28-36.
– reference: 477-484.
– reference: Lee CH, Wu SL, Chen JC, Li CC, Lo HY, Cheng WY, Lin JG, Chang YH, Hsiang CY, and Ho TY (2008)
– reference: 495-549.
– reference: Ischiropoulos H, Zhu L, and Beckman JS (1992) Peroxynitrite formation from macrophage-derived nitric oxide.
– reference: 151-157.
– reference: 1185-1198.
– reference: Economou M and Pappas G (2008) New global map of Crohn’s disease: genetic, environmental, and socioeconomic correlations.
– reference: Hsiang CY, Wu SL, and Ho TY (2005) Morin inhibited 12-
– reference: 801-807.
– reference: Hagan EC, Hansen WH, Fitzhugh OG, Jenner PM, Jones WI, Taylor JM, Long EL, Nelson AA, and Brouwer JB (1967) Food flavourings and compounds of related structure. II. Subacute and chronic toxicity.
– reference: Santosh Kumar SS, Priyadarsini KI, and Sainis KB (2004) Inhibition of peroxynitrite-mediated reactions by vanillin.
– reference: 221-224.
– reference: Cho JH (2008) The genetics and immunopathogenesis of inflammatory bowel disease.
– reference: Strober W, Fuss IJ, and Blumberg RS (2002) The immunology of mucosal models of inflammation.
– reference: Wallace JL and Keenan CM (1990) An orally active inhibitor of leukotriene synthesis accelerates healing in a rat model of colitis.
– reference: Ho TY, Chen YS, and Hsiang CY (2007) Noninvasive nuclear factor-κB bioluminescence imaging for the assessment of host-biomaterial interaction in transgenic mice.
– reference: Carlsen H, Moskaug JØ, Fromm SH, and Blomhoff R (2002) In vivo imaging of NF-κB activity.
– reference: 104-113.
– reference: Reinecker HC, Steffen M, Witthoeft T, Pflueger I, Schreiber S, MacDermott RP, and Raedler A (1993) Enhanced secretion of tumour necrosis factor-α, IL-6, and IL-1β by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn’s disease.
– reference: 783-797.
– reference: Neurath MF, Fuss I, Pasparakis M, Alexopoulou L, Haralambous S, Meyer zum Büschenfelde KH, Strober W, and Kollias G (1997) Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice.
– reference: 1441-1446.
– reference: 1603-1611.
– reference: Kamat JP, Ghosh A, and Devasagayam TP (2000) Vanillin as an antioxidant in rat liver mitochondria: inhibition of protein oxidation and lipid peroxidation induced by photosensitization.
– reference: 621-663.
– reference: Akagi K, Hirose M, Hoshiya T, Mizoguchi Y, Ito N, and Shirai T (1995) Modulating effects of ellagic acid, vanillin and quercetin in a rat medium term multi-organ carcinogenesis model.
– reference: invasion and
– reference: 3452-3457.
– reference: Joshi R, Kumar S, Unnikrishnan M, and Mukherjee T (2005) Free radical scavenging reactions of sulfasalazine, 5-aminosalicylic acid and sulfapyridine: mechanistic aspects and antioxidant activity.
– reference: 2766-2776.
– reference: 199-211.
– reference: S68-S82.
– reference: 257-262.
– reference: 559-566.
– reference: 139-145.
– reference: 998-1004.
– reference: Kirwin CJ and Galvin JB (1993) Ethers, in
– reference: Bradford MM (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding.
– reference: Mortelmans K, Haworth S, Lawlor T, Speck W, Tainer B, and Zeiger E (1986)
– reference: 174-181.
– reference: 505-515.
– reference: (Clayton GD and Clayton FE eds) pp 445-525, John Wiley & Sons, New York.
– reference: Neurath MF, Pettersson S, Meyer zum Büschenfelde KH, and Strober W (1996) Local administration of antisense phosphorothioate oligonucleotides to the p65 subunit of NF-κB abrogates established experimental colitis in mice.
– reference: Schreiber S, Nikolaus S, and Hampe J (1998) Activation of nuclear factor-κBin inflammatory bowel disease.
– reference: 1066-1071.
– reference: Holland N, Dong J, Garnett E, Shaikh N, Huen K, Harmatz P, Olive A, Winter HS, Gold BD, Cohen SA, et al. (2008) Reduced intracellular T-helper 1 interferon-γ in blood of newly diagnosed children with Crohn’s disease and age-related changes in Th1/Th2 cytokine profiles.
– ident: 10.1124/jpet.109.152835_bib12
  doi: 10.1016/S0015-6264(67)82961-4
– ident: 10.1124/jpet.109.152835_bib21
  doi: 10.1023/A:1007048313556
– ident: 10.1124/jpet.109.152835_bib6
  doi: 10.1016/j.mrfmmm.2004.02.024
– ident: 10.1124/jpet.109.152835_bib15
  doi: 10.1172/JCI119823
– ident: 10.1124/jpet.109.152835_bib11
  doi: 10.1111/j.1365-2672.2004.02275.x
– ident: 10.1124/jpet.109.152835_bib40
  doi: 10.1152/ajpgi.1990.258.4.G527
– ident: 10.1124/jpet.109.152835_bib36
  doi: 10.1016/S0016-5085(00)70007-2
– ident: 10.1124/jpet.109.152835_bib13
– ident: 10.1124/jpet.109.152835_bib32
  doi: 10.1038/nm0996-998
– ident: 10.1124/jpet.109.152835_bib8
  doi: 10.1038/nri2340
– ident: 10.1124/jpet.109.152835_bib41
  doi: 10.1016/S0031-9422(03)00149-3
– ident: 10.1124/jpet.109.152835_bib27
  doi: 10.1016/j.ejps.2005.01.015
– ident: 10.1124/jpet.109.152835_bib28
  doi: 10.1002/em.2860080803
– ident: 10.1124/jpet.109.152835_bib4
  doi: 10.1006/abio.1976.9999
– ident: 10.1124/jpet.109.152835_bib38
  doi: 10.1136/gut.42.4.477
– ident: 10.1124/jpet.109.152835_bib2
  doi: 10.1111/j.1572-0241.2000.03360.x
– ident: 10.1124/jpet.109.152835_bib25
  doi: 10.1142/S0192415X0800651X
– ident: 10.1124/jpet.109.152835_bib3
  doi: 10.1056/NEJM199704103361506
– ident: 10.1124/jpet.109.152835_bib5
  doi: 10.4049/jimmunol.168.3.1441
– ident: 10.1124/jpet.109.152835_bib9
  doi: 10.1002/ibd.20352
– ident: 10.1124/jpet.109.152835_bib39
  doi: 10.1146/annurev.immunol.20.100301.064816
– ident: 10.1124/jpet.109.152835_bib10
  doi: 10.4049/jimmunol.157.5.2174
– ident: 10.1124/jpet.109.152835_bib14
  doi: 10.1016/j.biomaterials.2007.07.005
– ident: 10.1124/jpet.109.152835_bib7
  doi: 10.1142/S0192415X08006235
– ident: 10.1124/jpet.109.152835_bib30
  doi: 10.1084/jem.182.5.1281
– ident: 10.1124/jpet.109.152835_bib20
  doi: 10.1080/10715760500177880
– ident: 10.1124/jpet.109.152835_bib17
  doi: 10.1016/j.bcp.2005.03.008
– ident: 10.1124/jpet.109.152835_bib18
  doi: 10.1016/0003-9861(92)90433-W
– ident: 10.1124/jpet.109.152835_bib34
  doi: 10.1111/j.1365-2249.1993.tb05997.x
– ident: 10.1124/jpet.109.152835_bib35
  doi: 10.1016/S0953-6205(00)00090-X
– ident: 10.1124/jpet.109.152835_bib19
  doi: 10.1016/0165-7992(87)90033-9
– ident: 10.1124/jpet.109.152835_bib31
  doi: 10.1002/eji.1830270722
– ident: 10.1124/jpet.109.152835_bib16
  doi: 10.1203/PDR.0b013e318163a897
– ident: 10.1124/jpet.109.152835_bib1
  doi: 10.1016/0304-3835(95)03833-I
– ident: 10.1124/jpet.109.152835_bib22
  doi: 10.1146/annurev.immunol.18.1.621
– ident: 10.1124/jpet.109.152835_bib29
– ident: 10.1124/jpet.109.152835_bib37
  doi: 10.1021/jf030319d
– ident: 10.1124/jpet.109.152835_bib24
  doi: 10.1002/path.1409
– ident: 10.1124/jpet.109.152835_bib23
– ident: 10.1124/jpet.109.152835_bib26
  doi: 10.1124/mol.108.049502
– ident: 10.1124/jpet.109.152835_bib33
  doi: 10.1016/0015-6264(77)90086-4
SSID ssj0014463
Score 2.2472327
Snippet Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and...
Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-κB (NF-κB) and...
Inflammatory bowel disease (IBD) is chronic inflammatory and relapsing disease of the gut. It has been known that activation of nuclear factor-kappaB...
SourceID proquest
pubmed
crossref
highwire
elsevier
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 370
SubjectTerms Animals
Benzaldehydes - therapeutic use
Colitis - chemically induced
Colitis - pathology
Colitis - prevention & control
Female
Mice
Mice, Inbred BALB C
Mice, Transgenic
Trinitrobenzenesulfonic Acid - toxicity
Title Vanillin Improves and Prevents Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice
URI https://dx.doi.org/10.1124/jpet.109.152835
http://jpet.aspetjournals.org/content/330/2/370.abstract
https://www.ncbi.nlm.nih.gov/pubmed/19423842
https://www.proquest.com/docview/67511401
Volume 330
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lb9NAEF5BuXBB5R3KYw-o4tAt8fqx9hFVrSIIpUgOhNPKXtvEEjhVG4PaX8_MPmynNOJxsaLV2nHyfR5_MzszS8hLHuYhD0TI4GUkGOh_zrLQLxj23itK5eV5haGB98fRZBa8nYfzPnVIV5es8n11eW1dyf-gCmOAK1bJ_gOy3UVhAD4DvnAEhOH4Vxh_yhoMlzRY63i2xP6xtuz_h65bW-HqjK73aS7BpGEmeqU3vMlUXTBwxltc_Fc6A06nxX63iXBOrfZ1Y1qxnvZtrk3XprXtAQaVXJ1O_9zq6OqiXrBp22cS2IKQ7Cc7WFy0fVJQbRIA6ozhnK_duA7nTs7rhn2p18IUSZck11lWjnGLsbFm5TVj1hz7dp2mHrjFxrj6ZouR340-D9Dog5eBzbFwR6fYtEBZb699_EEezaZTmR7O05vkFge_Ag3ju4_9shP4xroiw92X7QUFX_D6yuU3yZiuy_Rmj0Url3Sb3LEA0jeGP3fJjbK5R3ZPDJgXezQdALdHd-nJAOb7JHUko45kFKCnjmT0CsmoIxkdkoxaklG4DJLsAZkdHaYHE2a34mAK3kArxoOcVyLnSsVxlSiRhUUQjysvgwc98wUInDIpkkQkZSHyMKpAF3kgrPNq7MUqBA38kGw1y6Z8TGgQlFEmiijGSNrYU3HlK1EVoYqwO6TwR2Tf_bNS2T71uF3KN6n9VR5IhAIzJ6SBYkRedSecmhYtm6dyB5W0CtMoRwlc2nzSCweqHD5oEn6A5BJYCTMc1hKsMy65ZU25bM8luOMehjBG5JGhQH-HCTgyccCf_PHcHXK7f6Cekq3VWVs-AyW8yp9r9v4CkEe2NA
linkProvider Colorado Alliance of Research Libraries
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Vanillin+improves+and+prevents+trinitrobenzene+sulfonic+acid-induced+colitis+in+mice&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.au=Wu%2C+Shih-Lu&rft.au=Chen%2C+Jaw-Chyun&rft.au=Li%2C+Chia-Cheng&rft.au=Lo%2C+Hsin-Yi&rft.date=2009-08-01&rft.issn=1521-0103&rft.eissn=1521-0103&rft.volume=330&rft.issue=2&rft.spage=370&rft_id=info:doi/10.1124%2Fjpet.109.152835&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-3565&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-3565&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-3565&client=summon