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Isolation of gingerols and shogaols from ginger and evaluation of their chemopreventive activity on prostate cancer cells and anti-inflammatory effect on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear inflammation
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Title
Isolation of gingerols and shogaols from ginger and evaluation of their chemopreventive activity on prostate cancer cells and anti-inflammatory effect on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear inflammation
Name
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Ramji
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Divya
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Divya Ramji
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(authority = RULIB)
author
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chi
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Advisory Committee
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chi tang ho
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chair
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Huang
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Qingron
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Advisory Committee
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Qingron Huang
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internal member
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Rafi
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Mohamed
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Advisory Committee
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Mohamed Rafi
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internal member
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Huang
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Mou
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Advisory Committee
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Mou Tuan Huang
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(authority = RULIB)
outside member
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NamePart
Rutgers University
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degree grantor
Name
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NamePart
Graduate School-New Brunswick
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school
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Text
Genre
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theses
OriginInfo
DateCreated
(qualifier = exact)
2007
DateOther
(qualifier = exact);
(type = degree)
2007
Language
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(authority = ISO 639-3:2007);
(type = text)
English
PhysicalDescription
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electronic
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application/pdf
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text/xml
Extent
xvi, 177 pages
Abstract
(type = abstract)
Ginger, obtained from the rhizome of Zingiber officinale (Family Zingiberaceae), has been used extensively as a spice and in traditional medicine. The compounds in ginger primarily responsible for its medicinal properties are the gingerols. Gingerols can undergo dehydration, during storage and processing, to form the corresponding shogaols. Studies conducted so far have primarily focused on the biological activities of ginger and 6-gingerol. The main objectives of this research were to evaluate the anti-inflammatory and chemopreventive activities of gingerols and shogaols.
The crude ginger extract was subjected to column chromatography to obtain a mixture of gingerols, a mixture of shogaols, 6- gingerol, 8-gingerol and 6-shogaol which were characterized using high pressure liquid chromatography and nuclear magnetic resonance spectroscopy.
The anti-inflammatory activity of 6-gingerol and 6-shogaol was evaluated using the 12-O-tetradecanoylphorbol-13-acetate-induced mouse ear inflammatory model. Both 6-gingerol and 6-shogaol inhibited ear edema as well as the levels of proinflammatory cytokines.
The primary focus of this study was to evaluate the chemopreventive potential of these compounds on prostate cancer cells (LNCaP and PC-3). We hypothesized that gingerols and shogaols exhibit their chemopreventive potential through the modulation of the intrinsic pathway of apoptosis. Cell viability studies indicated that, among the compounds tested, 6-shogaol, 8-gingerol and shogaol mixture were the most effective in inhibiting cell growth in both cell lines. Morphological assessment, cell cycle, Annexin V staining and western blot analysis showed that 8-gingerol and 6-shogaol induced apoptosis in both the cell lines. Western blot analysis further confirmed our hypothesis that 8-gingerol and 6-shogaol induced apoptosis through activation of the intrinsic pathway of apoptosis as seen by caspase-9 cleavage. In addition, 8-gingerol and 6-shogaol induced the production of reactive oxygen species (ROS) which correlated well with the induction of apoptosis. This suggests that production of ROS could be one of the mechanisms of apoptosis induction by these compounds.
In conclusion, our study shows for the first time that gingerols and shogaols isolated from ginger were able to inhibit the growth of prostate cancer cells. 6-shogaol and 8-gingerol were able to induce apoptosis in both cell lines by activation of the intrinsic pathway of apoptosis.
The crude ginger extract was subjected to column chromatography to obtain a mixture of gingerols, a mixture of shogaols, 6- gingerol, 8-gingerol and 6-shogaol which were characterized using high pressure liquid chromatography and nuclear magnetic resonance spectroscopy.
The anti-inflammatory activity of 6-gingerol and 6-shogaol was evaluated using the 12-O-tetradecanoylphorbol-13-acetate-induced mouse ear inflammatory model. Both 6-gingerol and 6-shogaol inhibited ear edema as well as the levels of proinflammatory cytokines.
The primary focus of this study was to evaluate the chemopreventive potential of these compounds on prostate cancer cells (LNCaP and PC-3). We hypothesized that gingerols and shogaols exhibit their chemopreventive potential through the modulation of the intrinsic pathway of apoptosis. Cell viability studies indicated that, among the compounds tested, 6-shogaol, 8-gingerol and shogaol mixture were the most effective in inhibiting cell growth in both cell lines. Morphological assessment, cell cycle, Annexin V staining and western blot analysis showed that 8-gingerol and 6-shogaol induced apoptosis in both the cell lines. Western blot analysis further confirmed our hypothesis that 8-gingerol and 6-shogaol induced apoptosis through activation of the intrinsic pathway of apoptosis as seen by caspase-9 cleavage. In addition, 8-gingerol and 6-shogaol induced the production of reactive oxygen species (ROS) which correlated well with the induction of apoptosis. This suggests that production of ROS could be one of the mechanisms of apoptosis induction by these compounds.
In conclusion, our study shows for the first time that gingerols and shogaols isolated from ginger were able to inhibit the growth of prostate cancer cells. 6-shogaol and 8-gingerol were able to induce apoptosis in both cell lines by activation of the intrinsic pathway of apoptosis.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references (p. 152-175).
Subject
(authority = RUETD)
Topic
Food Science
Subject
(authority = ETD-LCSH)
Topic
Ginger
Subject
(authority = ETD-LCSH)
Topic
Cancer
Subject
(authority = ETD-LCSH)
Topic
Apoptosis
Subject
(authority = ETD-LCSH)
Topic
Cell death
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Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier
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rucore19991600001
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http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.13720
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doi:10.7282/T3VQ3348
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(displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
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ETD doctoral
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The author owns the copyright to this work.
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Copyright protected
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Open
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Divya Ramji
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Rutgers University. Graduate School-New Brunswick
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Non-exclusive ETD license
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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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