Abstract
Previous researches indicate that both Ge Gen Qin Lian Decoction and its active frictions improve insulin resistance of HepG2 cells, and the effect of active frictions is better than former. Further study shows that they improve insulin resistance through PI-3K pathway. In order to explore the mechanisms, the effect of Ge Gen Qin Lian Decoction and its active frictions on IRS-1 mRNA of insulin resistant HepG2 cells were studied. Insulin resistant model was established by incubating HepG2 cells for 24 hours in Dulbecco's modified Eagle's medium which free fatty acid concentration was 0.2mmol/L. The contents of glucose in the medium were determined by glucose oxidize method, and the mRNA expression of IRS-1 was detected by RT-PCR. The results indicate that the mRNA contents of IRS-1 decrease obviously in model group compared with normal group(P < 0.01). The mRNA contents of IRS-1 increase obviously in metformin group and in the middle, low dosage groups of the active frictions of Ge Gen Qin Lian Decoction compared with model group (P < 0.01), The mRNA contents of IRS-1 increase slightly in the high dosage group of the active frictions and Ge Gen Qin Lian Decoction group, but insignificantly compared with model group. Compared with the middle dosage group of the active frictions of Ge Gen Qin Lian Decoction, mRNA contents of IRS-1 decrease obviously in high and low dosage groups of the active frictions and the same dosage of Ge Gen Qin Lian Decoction group (P < 0.01). The results of this experiment suggest that Ge Gen Qin Lian Decoction and active frictions of Ge Gen Qin Lian Decoction improve insulin resistance in HepG2 cells, and that active frictions of Ge Gen Qin Lian Decoction improve insulin resistance in HepG2 cells partly by increasing the expression of IRS-1 mRNA. The mechanisms of Ge Gen Qin Lian Decoction improving insulin resistance are unknown.
Published Version
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