著者

國方 敏夫 河野 恵三 牛尾 慎平 福田 恵温

出版者

公益社団法人 日本薬学会

雑誌

YAKUGAKU ZASSHI (ISSN:00316903)

巻号頁・発行日

vol.131, no.11, pp.1667-1674, 2011-11-01 (Released:2011-11-01)

参考文献数

30

被引用文献数

1 1

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We previously reported that oral administration of NK-4, a criptocyanine dye, enhances interleukin (IL)-12-depend- ent interferon (IFN)-γ production by lipopolysaccharide (LPS)-stimulated mouse splenocytes. These findings raised a possibility that NK-4 potentiated IFN-γ production by T cells, natural killer (NK) cells or natural killer T (NKT) cells in response to IL-12 produced by macrophage and dendritic cells. To explore this possibility, we first analyzed percentages of T, NK or NKT cells in splenocytes of mice that were administered NK-4 orally for three days. The percentage of NKT cells in splenocytes from NK-4-treated mice was significantly (p<0.05) increased compared to vehicle-treated mice. When splenocytes were stimulated with α-galactosylceramide (α-GalCer), an NKT cell ligand, IFN-γ production by splenocytes from NK-4-treated mice tended to increase, while no difference in the IL-4 production and proliferation were observed between the vehicle- and NK-4-treated mice. When IFN-γ/IL-4 ratios were calculated in individual mice, the ratios were significantly (p<0.05) elevated in NK-4-treated mice. Furthermore, IL-12 production by α-GalCer-stimulated splenocytes from NK-4-treated mice was also significantly (p<0.05) increased. These results suggest that oral administration of NK-4 increases the population of type I NKT cells with potent IFN-γ-producing activities. Since IL-12 and IFN-γ have been shown to play important roles in anti-tumor immunity as well as in the defence against bacterial infection, our results further imply that NK-4 may provide a potential therapeutic tool in cancer immunotherapy.

著者

國方 敏夫 河野 恵三 牛尾 慎平 木村 英人 小川 智史 福田 恵温

出版者

日本生薬学会

雑誌

生薬學雜誌 (ISSN:13499114)

巻号頁・発行日

vol.65, no.1, pp.43-49, 2011-02-20

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Polyphenolic compounds have been shown to have growth inhibitory action on Helicobacter pylori (H. pylori). Previously, we demonstrated that seed shells of the Japanese horse chestnut (Aesculus turbinata BLUME) are rich in polymerized polyphenol compounds. In this study, we have examined the effects of polyphenolic compounds from the seed shells of the Japanese horse chestnut on adherence of H. pylori to MKN 45 cells, a human stomach cancer cell line. Polyphenolic compounds, which are composed of monomeric forms of (+)-catechin and (-)-epicatechin and polymeric proanthocyanidins, reportedly inhibited the colony formation of H. pylori on agar plates (minimal inhibitory concentration: 180μg/ml). Interestingly, the polyphenolic compounds also inhibited adherence of H. pylori to MKN 45 cells at concentrations that showed no growth inhibitory action on H. pylori. When the polyphenolic compounds were further fractionated by gel filtration chromatography depending on the degrees of polymerization, fractions including polymeric proanthocyanidins exhibited higher inhibitory effects compared with a fraction containing lower-molecular weight compounds. MKN 45 cells reportedly produced IL-8 spontaneously, and IL-8 production was increased by H. pylori infection. We found that polymeric proanthocyanidins significantly and dose-dependently reduced the H. pylori-induced IL-8 production as well as the spontaneous IL-8 production. Our results raise the possibility that polymeric proanthocyanidins contained in the seed shells of the Japanese horse chestnut may prevent infection and inflammatory responses by H. pylori.