Figure 6.

Rutin was a hypoglycemic component of DLE working through IGF1R. RT-qPCR validation of rutin-mediated (A) IGF1R and (B) FOXO1-related genes in HepG2 cells treated with 50 μmol/L rutin for 24 h (n = 3). (C) The inhibitory effects of rutin on the transcriptional activity of the G6PC and PCK1 promoters (n = 3). (D) Dose responsive inhibitory effects of rutin on glucose production. HepG2 cells were treated with indicated concentrations of rutin for 24 h, followed by glucose production analysis. Data were analyzed using linear regression (n = 3). (E) Western blot showing FOXO1, AKT, and GSK3β expression in HepG2 cells treated with rutin for 24 h (n ≥ 3), (F) 30 or 60 min (n = 5), the data were quantified by ImageJ. (G–I) RT-qPCR results of FOXO1 downstream gene PCK1 (n = 4), G6PC (n = 4), and PDK4 (n = 3) in HepG2 cells. Cells were treated by DLE or rutin with or without IGF1R inhibitor GSK1904529A for 24 h, respectively. All the data are shown as the mean ± SD. Statistical analyses were conducted using paired Student's t-tests. ∗P < 0.05, ∗∗P < 0.01 vs. the DMSO group, ns means not significant. PCK1, phosphoenolpyruvate carboxykinase 1; PDK4, pyruvate dehydrogenase lipoamide kinase isozyme 4; G6PC, glucose-6-phosphatase.