Fig 2: Glucose tolerance and insulin tolerance in HUA rats. (A) Glucose tolerance tests were performed to detect glucose tolerance in HUA and CON rats (n = 10 per group). (B) Insulin tolerance tests were performed to detect glucose tolerance in HUA and control rats. (C) About 30 µg protein were loaded and the expression of p-IRS-1 (PY896), p-IRS-2 (S731), p-PI3K (P85), and p-Akt (Ser473) were measured by Western blot in the adipose tissue of HUA and CON rats. The representative views are shown in the left panel and densitrometric quantification analysis for RBP4 is shown in the right panel. Results are represented by mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001.

Fig 3: Circ_0000215 modulates PIK3R1 through sponging miR-512-5p. (A) Venn diagram was employed to show the targets of miR-512-5p predicted by TargetScan, miRWalk, miRDB and mirDIP. (B) The schematic diagram showed the predicted targets of miR-512-5p. (C) qRT-PCR was performed to detect PIK3R1 expression in 32 pairs of NPC tissues and normal tissues adjacent to cancer. (D) The schematic diagram showed the binding sites between miR-512-5p and PIK3R1 3'UTR. (E) Dual-luciferase reporter gene assay was performed to validate the binding sites between miR-512-5p and PIK3R1 3'UTR. (F) Western blot was utilized to detect the effects of circ_0000215 and miR-512-5p on PIK3R1 expression in HONE1 and CNE-2 cells. The significance of difference was determined by Student’s t-test or one-way ANOVA.**P < 0.01, and ***P < 0.001, ns differences were not statistically significant. Data from three independent experiments were expressed as mean ± standard deviation.

Fig 4: Swainsonine impeded the activation of PI3K/AKT/mTOR pathway by repressing miR-92a expression. After transfection and treatment, a and b p/t-phosphatidylinositol-3 kinase (PI3K) and p/t-protein kinase B (AKT) were appraised by exploiting western blot assay; c and d p/t-mammalian target of rapamycin (mTOR) and p/t-phosphorylated and total 70-kDa ribosomal protein S6 kinase (p70S6K) were appraised by utilizing western blot. *p < 0.05; ***p < 0.001

Fig 5: Acacetin improved gastrointestinal motility by inhibiting the activation of the PI3K-AKT signaling pathway. (a) The expression of the PI3K-AKT signaling pathway-related proteins PI3K, p-PI3K, AKT, and p-AKT was detected by Western blot. (b) IHC was used to measure the expression of PI3K, p-PI3K, AKT, and p-AKT in gastric antrum tissues. CG: control group; MG: model group; LAG: low-dose Acacetin group; MAG: middle-dose Acacetin group; HAG: high-dose Acacetin group; MPG: Mosapride group; *P < 0.05 vs. CG; #P < 0.05 vs. MG; scale bar = 25 µm; the magnification was 400 times; scale bar = 100 µm; the magnification was 100 times.