【摘要】 旨在探讨环氧二十碳三烯酸(EETs)是否可改善由HepG2细胞模拟的小鼠2型糖尿病模型中的胰岛素抵抗。用HepG2细胞建立胰岛素抵抗(IR)模型，用CCK-8法测定细胞活力，用葡萄糖氧化酶法测定细胞上清液中葡萄糖消耗量，通过Western blot检测PI3K/AKT及其磷酸化蛋白表达。结果表明，当胰岛素浓度为0.1μmol/L时，HepG2细胞的葡萄糖消耗量最低，产生的胰岛素抵抗程度最高；EETs、TPPU干预后，IR-HepG2细胞的葡萄糖消耗量均有所提升，表明可以有效改善IR-HepG2细胞的胰岛素抵抗程度；测定发现IR-HepG2细胞中的p-PIK/PI3K和p-AKT/AKT比值显著降低，而EETs组和TPPU组的PIK/PI3K和p-AKT/AKT比值显著上升，表明EETs能够通过激活PI3K/AKT信号通路改善胰岛素抵抗。更多还原

【Abstract】 The aim of this study is to investigate how EETs improve insulin resistance in a mouse type 2 diabetes model simulated by HepG2 cells through their mechanisms of action.Insulin resistance(IR) model was established using HepG2 cells; cell viability was measured using the CCK-8 method; glucose consumption in the cell supernatant was determined using the glucose oxidase method; and the expressions of PI3K/AKT and their phosphorylated proteins were detected by Western blot.The study found that when the insulin concentration was 0.1 μmol/L,the glucose consumption of HepG2 cells was the lowest, resulting in the highest degree of insulin resistance; after intervention with EETs and TPPU,the glucose consumption of IR-HepG2 cells increased, indicating effective improvement in the insulin resistance of IR-HepG2 cells; measurements revealed a significant decrease in the p-PIK/PI3K and p-AKT/AKT ratios in IR-HepG2 cells, while the PIK/PI3K and p-AKT/AKT ratios in the EETs and TPPU groups significantly increased, suggesting that EETs can improve insulin resistance by activating the PI3K/AKT signaling pathway.更多还原