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NFKB Activity Decreased In BALB/c Mice With High Fat Diet And Fructose

机译:NFKB活性在BALB / C小鼠中减少,具有高脂肪饮食和果糖

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Excessive consumption of fat and fructose leads to obesity due to lipid accumulation. The excessive lipid causes hypertrophy in the adipocytes which lead to cell death. Consequently, dead adipocytes will produce adipokines, which cause macrophages and lymphocytes to infiltrate into the adipose tissue, elevating pro-inflammatory cytokines, thus triggering the production of pro-inflammatory cytokines through NFκB activity. Elicited soybeans extract (ESE) with bacteria and light contain Glyceollin and Isoflavones, which inhibit the activation of NFKB and reduce plasma cholesterol levels by upregulating cholesterol metabolism. This study aimed to analyze the effect of ESE against the relative number of CD4~+ NFκB ~+ cells in BALB/c mice spleen after administrated by high-fat diet food and fructose (HFD) for 20 weeks. Mice were given orally with ESE after administrated by HFD at dose 78 mg/kgBW (Dl), 104 mg/kgBW (D2), and 130 mg/kgBW (D3) for 4 weeks. This study also used positive control (HFD mice model without ESE treatment) and normal mice. Identification of NFKB activation was conducted using Flowcytometry analytical methods. Our result indicated that ESE could decrease significantly activation of NFκB in CD4 cell compare than positive control. The optimum dose that can decrease the relative number of CD4~+ NFκB~+cells is dose 3.
机译:由于脂质积累,过量消耗脂肪和果糖导致肥胖。过量的脂质导致脂肪细胞中的肥厚,导致细胞死亡。因此,死亡脂肪细胞将产生脂肪因子,其导致巨噬细胞和淋巴细胞渗透到脂肪组织中,升高促炎细胞因子,从而通过NFκB活性引发促炎细胞因子的产生。具有细菌和光的引发大豆提取物(ESE)含有甘氨酸素和异黄酮,其通过上调胆固醇代谢来抑制NFKB的活化并降低血浆胆固醇水平。本研究旨在通过高脂饮食食品和果糖(HFD)施用20周后,分析ESE对BALB / C小鼠脾脏的相对数量的CD4〜+NFκB〜+细胞的影响。在剂量78mg / kgbw(D1),104mg / kgbw(d2),130mg / kgbw(d3)的剂量78mg / kgbw(dl),104mg / kgbw(d3)下给予ESE,对小鼠进行口服。该研究还使用阳性对照(没有ESE治疗的HFD小鼠模型)和正常小鼠。使用流裂化测定方法进行NFKB活化的鉴定。我们的结果表明,ESE可以比阳性对照比较的CD4细胞中NFκB显着激活。可以降低CD4〜+NFκB〜+细胞相对数量的最佳剂量是剂量3。

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