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KMID : 1239920200140020109
Nutrition Research and Practice
2020 Volume.14 No. 2 p.109 ~ p.116
Effect of saccharin on inflammation in 3T3-L1 adipocytes and the related mechanism
Kim Hye-Lin

Ha Ae-Wha
Kim Woo-Kyoung
Abstract
BACKGROUND/OBJECTIVES: Excessive intake of simple sugars induces obesity and increases the risk of inflammation. Thus, interest in alternative sweeteners as a sugar substitute is increasing. The purpose of this study was to determine the effect of saccharin on inflammation in 3T3-L1 adipocytes.

MATERIALS/METHODS: 3T3-L1 preadipocytes were differentiated into adipocytes. The adipocytes were treated with saccharin (0, 50, 100, and 200 ¥ìg/mL) for 24 h. Inflammation was induced by exposure of treated adipocytes to lipopolysaccharide (LPS) for 18 h and cell proliferation was measured. The concentration of nitric oxide (NO) was measured by using Griess reagent. Protein expressions of nuclear factor kappa B (NF-¥êB) and inhibitor ¥êB (I¥êB) were determined by western blot analysis. The mRNA expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin 1¥â (IL-1¥â), interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-¥á (TNF-¥á) were determined by real-time PCR.

RESULTS: Compared with the control group, the amount of NO and the mRNA expression of iNOS in the LPS-treated group were increased by about 17.6% and 46.9%, respectively, (P < 0.05), and those parameter levels were significantly decreased by saccharin treatment (P < 0.05). Protein expression of NF-¥êB was decreased and that of I¥êB was increased by saccharin treatment (P < 0.05). Saccharin decreased the mRNA expression of COX-2 and the inflammation cytokines (IL-1¥â, IL-6, MCP-1, and TNF-¥á) (P < 0.05).

CONCLUSIONS: The results of this study suggest that saccharin can inhibit LPS-induced inflammatory responses in 3T3-L1 adipocytes via the NF-¥êB pathway.
KEYWORD
Saccharin, inflammation, cytokine, adipocytes, NF-kappa B
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