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...
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Published in | The Journal of pharmacology and experimental therapeutics Vol. 330; no. 2; pp. 370 - 376 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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United States
Elsevier Inc
01.08.2009
American Society for Pharmacology and Experimental Therapeutics |
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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. |
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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 |
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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 |
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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 |
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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... |
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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 |
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