Novel guggulsterone derivative GG-52 inhibits NF-κB signaling in intestinal epithelial cells and attenuates acute murine colitis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-03-01

AUTHORS

Jung Mogg Kim, Hyoun Woo Kang, Mi Yeon Cha, Doyoung Yoo, Nayoung Kim, In-Kyoung Kim, Jeounghun Ku, Sunil Kim, Sang-Ho Ma, Hyun Chae Jung, In Sung Song, Joo Sung Kim

ABSTRACT

We already showed that the plant sterol guggulsterone has been reported to inhibit nuclear factor-κB (NF-κB) signaling in intestinal epithelial cells (IECs) and to attenuate dextran sulfate sodium (DSS)-induced colitis. This study investigates the anti-inflammatory effects of novel guggulsterone derivatives on IEC and preventive and therapeutic murine models of DSS-induced colitis. Novel guggulsterone derivates with high lipophilicity were designed and four derivates, including GG-46, GG-50B, GG-52, and GG-53, were synthesized. Two guggulsterone derivatives, GG-50B and GG-52, significantly inhibited the activated NF-κB signals and the upregulated expression of interleukin-8 (IL-8) in COLO 205 cells stimulated with tumor necrosis factor-α (TNF-α). Pretreatment with GG-50B and GG-52 attenuated the increased IκB kinase (IKK) and IκBα phsophorylation induced by TNF-α. In preventive and therapeutic models of murine colitis, administration of GG-52 significantly reduced the severity of DSS-induced colitis, as assessed by disease activity index, colon length, and histology. In contrast, GG-50B did not show a significant reduction in the colitis severity. Moreover, the efficacy on attenuating colitis by GG-52 was comparable to that by sulfasalazine or prednisolone. These results indicate that the novel guggulsterone derivative GG-52 blocks NF-κB activation in IEC and ameliorates DSS-induced acute murine colitis, which suggests that GG-52 is a potential therapeutic agent for the treatment of inflammatory bowel diseases. More... »

PAGES

1004-1015

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/labinvest.2010.54

DOI

http://dx.doi.org/10.1038/labinvest.2010.54

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1028780771

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/20195240


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40 GG-52
41 GG-52 blocks NF-κB activation
42 GG-52 inhibits NF-κB
43 GG-53
44 IκB kinase
45 IκBα phsophorylation
46 NF-κB
47 NF-κB activation
48 NF-κB signal
49 Novel guggulsterone
50 Novel guggulsterone derivative GG-52 inhibits NF-κB
51 TNF
52 activation
53 activity index
54 acute murine colitis
55 administration
56 agents
57 anti-inflammatory effects
58 blocks NF-κB activation
59 bowel disease
60 cells
61 colitis
62 colitis severity
63 colon length
64 contrast
65 derivates
66 derivative GG-52 blocks NF-κB activation
67 derivative GG-52 inhibits NF-κB
68 derivatives
69 dextran sulfate sodium
70 disease
71 effect
72 efficacy
73 epithelial cells
74 expression
75 factors
76 guggulsterone
77 guggulsterone derivative GG-52 blocks NF-κB activation
78 guggulsterone derivative GG-52 inhibits NF-κB
79 guggulsterone derivatives
80 high lipophilicity
81 histology
82 index
83 induced colitis
84 inflammatory bowel disease
85 inhibits NF-κB
86 interleukin-8
87 intestinal epithelial cells
88 kinase
89 length
90 lipophilicity
91 model
92 murine colitis
93 murine model
94 necrosis factor
95 novel guggulsterone derivative GG-52 blocks NF-κB activation
96 novel guggulsterone derivatives
97 phsophorylation
98 plant sterol guggulsterone
99 potential therapeutic agent
100 prednisolone
101 pretreatment
102 reduction
103 results
104 severity
105 severity of DSS
106 signals
107 significant reduction
108 sodium
109 sterol guggulsterone
110 study
111 sulfasalazine
112 sulfate sodium
113 therapeutic agents
114 therapeutic model
115 therapeutic murine models
116 treatment
117 tumor necrosis factor
118 upregulated expression
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