Kim Hye Lin, Ha Ae Wha, Kim Woo Kyoung
Department of Food Science and Nutrition, Dankook University, 119, Dandae-ro, Dongnam-gu, Cheonan-si, Chungnam 31116, Korea.
Department of Food Science and Nutrition, Natural Nutraceuticals Industrialization Research Center, DanKook University, Chungnam 31116, Korea.
Nutr Res Pract. 2020 Apr;14(2):109-116. doi: 10.4162/nrp.2020.14.2.109. Epub 2020 Jan 21.
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 µg/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-κB) and inhibitor κB (IκB) were determined by western blot analysis. The mRNA expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin 1β (IL-1β), interleukin 6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) were determined by real-time PCR.
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, ( < 0.05), and those parameter levels were significantly decreased by saccharin treatment ( < 0.05). Protein expression of NF-κB was decreased and that of IκB was increased by saccharin treatment ( < 0.05). Saccharin decreased the mRNA expression of COX-2 and the inflammation cytokines (IL-1β, IL-6, MCP-1, and TNF-α) ( < 0.05).
The results of this study suggest that saccharin can inhibit LPS-induced inflammatory responses in 3T3-L1 adipocytes via the NF-κB pathway.
背景/目的：过量摄入单糖会导致肥胖并增加炎症风险。因此，人们对作为糖替代品的甜味剂的兴趣日益增加。本研究的目的是确定糖精对3T3-L1脂肪细胞炎症的影响。
材料/方法：将3T3-L1前脂肪细胞分化为脂肪细胞。将脂肪细胞用糖精（0、50、100和200μg/mL）处理24小时。通过将处理后的脂肪细胞暴露于脂多糖（LPS）18小时来诱导炎症，并测量细胞增殖。使用格里斯试剂测量一氧化氮（NO）的浓度。通过蛋白质印迹分析确定核因子κB（NF-κB）和抑制蛋白κB（IκB）的蛋白表达。通过实时PCR确定诱导型一氧化氮合酶（iNOS）、环氧化酶-2（COX-2）、白细胞介素1β（IL-1β）、白细胞介素6（IL-6）、单核细胞趋化蛋白-1（MCP-1）和肿瘤坏死因子-α（TNF-α）的mRNA表达。
与对照组相比，LPS处理组中NO的量和iNOS的mRNA表达分别增加了约17.6%和46.9%（P<0.05），而糖精处理显著降低了这些参数水平（P<0.05）。糖精处理使NF-κB的蛋白表达降低，IκB的蛋白表达增加（P<0.05）。糖精降低了COX-2和炎症细胞因子（IL-1β、IL-6、MCP-1和TNF-α）的mRNA表达（P<0.05）。
本研究结果表明，糖精可通过NF-κB途径抑制LPS诱导的3T3-L1脂肪细胞炎症反应。
