蓝莓花色苷提取物干预人肝癌细胞对葡萄糖消耗的作用研究

Blueberry Anthocyanin Extracts Regulate Glucose Consumption in HepG2 Cells

摘要:

探究蓝莓花色苷提取物对胰岛素抵抗的人肝癌细胞HepG2细胞对葡萄糖消耗的干预作用。利用MTT实验筛选得到3个品种蓝莓花色苷提取物的最适作用浓度；筛选胰岛素和葡萄糖诱导HepG2细胞产生胰岛素抵抗的最佳浓度；以MTT矫正细胞数量，用葡萄糖氧化酶法检测细胞培养基中葡萄糖的变化来研究蓝莓花色苷提取物的对细胞胰岛素抵抗的干预作用。北陆花色苷提取物在低于200 μg/mL的浓度时，灿烂和园蓝花色苷提取物在低于100 μg/mL的浓度时，对HepG2细胞活力无明显影响；以诱导剂胰岛素的浓度为1×10-8 mol/L，孵育24 h作为诱导条件，其模型效果较佳、对细胞活力改变小且稳定性好；3个品种的蓝莓花色苷提取物在7.8125~31.25 μg/mL浓度时，可不同程度促进正常HepG2细胞和胰岛素抵抗的HepG2细胞对葡萄糖的消耗量，且与剂量成正比关系，在31.25 μg/mL达到促进最大值，与模型组比较均有极显著差异，糖消耗量分别增加了60%、65%和88%。三个品种的蓝莓花色苷提取物均能较好的预防和改善胰岛素抵抗HepG2细胞对葡萄糖的利用。

Abstract:

The regulation of glucose consumption in insulin-resistant hepatoma cell line HepG2 with blueberry anthocyanin extracts was investigated. The optimum concentration of blueberry anthocyanin extracts was screened by MTT assay. Different concentrations of insulin and glucose were performed to induce insulin resistance in HepG2 cells. The number of cells was corrected by MTT, and contents of glucose in medium were detected by glucose oxidase method. Changes in glucose in the medium reflected the intervention of the blueberry anthocyanin extract on cellular insulin resistance. MTT results showed that and there was no significant effect on the activity of HepG2 cells at concentrations below 200 μg/mL of the extracts of NL BAEs and that below 100 μg/mL of the extracts of BW BAEs and GB BAEs. With the inducing agent insulin concentration of 1×10-8 mol/L and incubation for 24 h as the induction condition, the model was effective, while the cell viability had no significant change and the stability was good. It could promote glucose consumption in normal HepG2 cells and insulin-resistant HepG2 cells at the concentration of 7.8125~31.25 μg/mL of three varieties of blueberry anthocyanin extracts and showed a dose-effect relationship. It had a maximum at 31.25 μg/mL. Compared to the model group, sugar consumptions of extracts of NL BAEs, BW BAEs and GB BAEs had increased by 60%, 65% and 88%, respectively. Three varieties of blueberry anthocyanin extract could prevent and improve the utilization of glucose by insulin-resistant HepG2 cells.