Anti-inflammatory and Anti-tumorigenic Effects of Açai Berry in Helicobacter felis-infected mice
- Author(s)
- Ju Yup Lee; Nayoung Kim; Yoon Jeong Choi; Ryoung Hee Nam; Seonmin Lee; Min Hee Ham; Ji Hyung Suh; Yoon Jin Choi; Hye Seung Lee; Dong Ho Lee
- Keimyung Author(s)
- Lee, Ju Yup
- Department
- Dept. of Internal Medicine (내과학)
- Journal Title
- Journal of Cancer Prevention
- Issued Date
- 2016
- Volume
- 21
- Issue
- 1
- Keyword
- Açai (Euterpe oleracea); Stomach; Helicobacter felis; Inflammation
- Abstract
- Background: The aim of this study was to evaluate the anti-inflammatory and anti-tumorigenic effect of açai berry after chronic
Helicobacter felis colonization in the stomachs of C57BL/6 mice.
Methods: A total of 57 four-week-old female C57BL/6 mice (18 control mice and 39 experimental mice) were used. The mice were
administered orogastrically with vehicle only or vehicle containing H. felis, 5 times every other day. After inoculation of H. felis, mice
were fed either a standard or an açai-containing diet and then sacrificed at 4, 24, and 52 weeks. The infection status and degree
of inflammation were determined by culture and histopathology. The level of gastric mucosal myeloperoxidase (MPO), TNF-, and
interleukin-1 (IL-1) were measured by ELISA.
Results: At 24 weeks after inoculation, mucosal atrophy and mucous metaplasia appeared in all infected mice. At 52 weeks after
inoculation, dysplastic change was noted in 10%, 25%, and 50% of mice in the H. felis-control, H. felis-açai 5%, and H. felis-açai 10%
groups, respectively. The neutrophil, monocyte, atrophy, and metaplasia grades of infected mice showed no significant difference among
the H. felis-infected groups. H. felis-infected mice fed with açai berry showed no significant difference compared with H. felis-infected
control mice in gastric mucosal MPO, TNF-, and IL-1 levels.
Conclusions: H. felis that colonized the stomachs of C57BL/6 mice provoked inflammation, and induced mucosal atrophy, metaplasia,
and dysplasia. However, açai berry did not effectively prohibit the gastric carcinogenesis which was induced by chronic H. felis infection.
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