Objective:To observe the effect of Gynura divaricata on mRNA expressions of insulin receptor (InsR) and glucose transporter 4 (GLUT4)

and protein expressions of protein kinase B (PKB) and glycogen synthase kinase-3β (GSK-3β) on insulin resistance in HepG2 cells

in order to discuss the molecular mechanism of insulin resistance after intervention. Method:Insulin-induced HepG2 cells were used to produce insulin resistance. The experiment included blank control group

model group

high-dose and low-dose G. divaricata hot water extracts (GDE

1.0

0.5 g·L-1) groups

high-dose and low-dose G. divaricata flavonoids (GDF

0.2

0.1 g·L-1) groups

high-dose and low-dose G. divaricata alkaloid(GDA

0.1

0.05 g·L-1) groups. Glucose oxidase method was used to detect the content of glucose in supernatant of HepG2 cell culture medium; mRNA expressions of insulin receptor (InsR) and glucose transporter 4 (GLUT4) in HepG2 cells were detected by Real-time PCR; and Western blot was used to detect protein expressions of kinase B (PKB) and GSK-3β in HepG2 cells. Result:Compared with model control group

the glucose content of supernatant was significantly decreased in 1.0

0.5 g·L-1 GDE groups (P<0.01)

and the glucose content was significantly decreased in supernatant of 0.2 g·L-1GDF group (P<0.05); the mRNA expressions of INSR and GLUT4 in GDE and GDF groups increased significantly (P<0.05); the protein expression of PKB was significantly increased (P<0.05)

and the protein expression of GSK-3β was significantly reduced in GDE group (P<0.05)

the protein expression of PKB was significantly increased(P<0.01)and the protein expression of GSK-3β decreased significantly in GDF group (P<0.01). Conclusion:Gynura divaricata may improve insulin resistance HepG2 cells' uptake of glucose. Its mechanism may be related to the up-regulation of InsR

GLUT4 mRNA expression and PKB protein expression

and the reduction of GSK-3β protein expression in insulin resistant HepG2 cells.