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Effects of inotilone on inflammation and inflammation-associated tumorigenesis
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Effects of inotilone on inflammation and inflammation-associated tumorigenesis
Identifier
ETD_2965
Identifier
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http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056479
Language
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eng
Genre
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theses
Subject
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(authority = RUETD)
Topic
Food Science
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Inflammation--Mediators
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Anti-inflammatory agents
Subject
(ID = SBJ-4);
(authority = ETD-LCSH)
Topic
Carcinogenesis
Abstract
(type = abstract)
Inflammation, a complex process, involving numerous mediators of cellular and plasma origins, is considered to be a critical factor in many human diseases and conditions, including obesity, cardiovascular diseases, diabetes, aging, and cancers. Inotilone, a secondary metabolite recently found in the dietary Inonotus mushroom, has been reported as a potent inflammatory inhibitor in test tube. However, its inhibitory effect at cellular level as well as in animal model remain unclear. The anti-inflammatory effects of inotilone were investigated in vitro using lipopolysaccharide (LPS)-stimulated murine macrophage. Inotilone was shown to inhibit nitric oxide (NO) and prostaglandin E2 (PGE2) production through modulating inducible nitric oxide synthase (iNOS) expression and cyclooxygenase 2 (COX 2) enzyme activity, respectively. It is also found that inotilone can only suppressed the expression of iNOS but not COX 2. This divergence may origin from the differential effect of inotilone on transcription factors, nuclear factor κB (NF κB) and CCAAT enhancer-binding protein (C/EBP). However, this differential effect was not found in the in vivo study employing 12 O tetradecanoylphorbol 13 acetate (TPA)-treated mouse skin. This finding suggested that the effects of inotilone on C/EBPβ expression may be cell type- or stimuli-specific. The inhibitory effects of inotilone were also observed on the activation of phosphatidylinositol 3-kinase/Akt (PI3K/Akt), extracellular signal-regulated protein kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) signaling pathways both in vitro and in vivo. Furthermore, the ability of inotilone to prevent inflammation-associated tumorigenesis was also evaluated using a classical two-stage mouse skin carcinogenesis model. After initiation of 7,12 dimethylbenz[a]nthracene (DMBA), applying inotilone topically before each TPA treatment was found to reduce the incidence and multiplicity of papillomas at 20th week. Taken together, the results suggest that inotilone has potential to be developed into an effective chemopreventive agent for the treatment of a variety of inflammatory diseases, especially the prevention and treatment of epithelial skin cancer.
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electronic resource
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xii, 73 p. : ill.
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Note
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Ph.D.
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Includes bibliographical references
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Includes vita
Note
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by Yu-Ching Kuo
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Kuo
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Yu-Ching
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1980-
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author
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Yu-Ching Kuo
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CHI-TANG
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chair
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HUANG
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QINGRONG
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MOU-TUAN HUANG
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Rutgers University
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Graduate School - New Brunswick
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OriginInfo
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2010
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2010-10
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xx
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Rutgers University Electronic Theses and Dissertations
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ETD
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Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
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NjNbRU
Identifier
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doi:10.7282/T3C24W5Q
Genre
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ETD doctoral
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Rights
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The author owns the copyright to this work.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
RightsHolder
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Name
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Kuo
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Yu-Ching
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DateTime
2010-09-30 14:16:03
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Yu-Ching Kuo
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Rutgers University. Graduate School - New Brunswick
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Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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DateTime
2010-10-31
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 2nd, 2011.
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