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자료유형
학술저널
저자정보
Zhang, Xulong (Department of Immunology, School of Basic Medical Sciences, Capital Medical University) Bo, Agula (Department of Public Health, Inner Mongolia Medical University) Chi, Baofeng (Department of Public Health, Inner Mongolia Medical University) Xia, Yuan (Department of Public Health, Inner Mongolia Medical University) Su, Xiong (Department of Public Health, Inner Mongolia Medical University) Sun, Juan (Department of Public Health, Inner Mongolia Medical University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제16권 제1호
발행연도
2015.1
수록면
71 - 76 (6page)

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Magnesium sulfate is widely used as a food additive and as an orally administered medication. The aim of this study was to evaluate the possible cytotoxicity of magnesium sulfate on AGS human gastric adenocarcinoma cells and gastric mucosa in mice. A trypan blue exclusion assay was used to determine the reduction in viability of AGS cells exposed to magnesium sulfate, and then effects on cell proliferation were quantified. The role of magnesium sulfate-mediated pro-inflammatory cytokine production in AGS cells was also investigated. mRNA expression for IL-$1{\beta}$, IL-6, IL-8, and TNF-${\alpha}$ was determined by RT-PCR, and secretion of these cytokines was measured by ELISA. Immunohistochemical evaluation of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ expression was conducted in mouse gastric mucosa. Addition of 3 to 50 mM magnesium sulfate to AGS cells inhibited both cell proliferation and cell viability in a dose-dependent manner. Magnesium sulfate had little effect on production of IL-$1{\beta}$ or IL-6 but significantly inhibited production of IL-8. The animal model demonstrated that magnesium sulfate induced production of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$. These preliminary data suggest that magnesium sulfate had a direct effect on the stomach and initiates cytotoxicity in moderate concentrations and time periods by inhibiting viability a nd proliferation of AGS cells and by regulating expression and/or release of pro-inflammatory cytokines.

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