XU Hua-rong, LI Li-qi, LIU Yang, YAO Shao-cheng, SHEN Man-yun, CAO Qing, TANG Zhi-wei, RUAN Jin-lan. The mechanism of purple potato anthocyanins improve the insulin resistance model of HepG2 cells*[J]. Science and Technology of Food Industry, 2018, 39(5): 319-324.
Citation: XU Hua-rong, LI Li-qi, LIU Yang, YAO Shao-cheng, SHEN Man-yun, CAO Qing, TANG Zhi-wei, RUAN Jin-lan. The mechanism of purple potato anthocyanins improve the insulin resistance model of HepG2 cells*[J]. Science and Technology of Food Industry, 2018, 39(5): 319-324.

The mechanism of purple potato anthocyanins improve the insulin resistance model of HepG2 cells*

  • Objective:To observe the effect of purple potato anthocyanin in HepG2 cell insulin resistance model on glucose metabolism and explore its mechanism. Methods:High concentration glucose medium as the induction factor to induce the HepG2 cells establishing insulin resistance cell model. The effects of purple potato anthocyanins on glucose consumption,cell viability and protein expression of insulin signaling pathway were investigated though the glucose oxidase method,tetrazolium colorimetric assay(MTT)and Western blot.Compared with the blank control group,the difference of absorbance was greatest when the glucose concentration was 50 mmol/L,so 50 mmol/L glucose medium was chosed to establish insulin resistance cell model. When the concentration was 40~100 μg/mL of anthocyanin which was used to treating the insulin resistance cell model,the glucose consumption could be as high as 19.55 mmol/L which was significantly(p<0.05)higher than that of the model control group. When the concentration of anthocyanin was 40~100 μg/mL,the cell survival rate could be kept at 80%,with less cytotoxicity. Anthocyanins could regulate the stuations of levels decreasing of IR,IRS-1,IRS-2 due to high concentration of glucose,could reduce the expression level of p-IRS-1 and also prevent the decrease of GLUT-2 level. Conclusion:Purple potato anthocyanins could improve the insulin signal pathway inhibition situation of HepG2 cell insulin resistance model and improve the glucose metabolism situation of insulin resistance model.
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