Fig 2: The effect of NCTS on modulation of insulin resistance (IR) related to PTP1B in db/db mice. (A) NCTS enhanced the serum levels of insulin (n = 6). (B) NCTS decreased the value of homeostasis model of insulin resistance (HOMA-IR) (n = 6). (C) NCTS suppressed the expressions of PTP1B demonstrated by immunohistochemistry (n = 3). NCTS enhanced the phosphorylation of insulin receptor substrate 1 (IRS1) and protein kinase B (AKT) and suppressed the expressions of PTP1B in the (D) liver and (E) muscle of db/db mice (n = 3). Quantification data were normalized to a/ß-actin or the corresponding total protein concentration, and expressed as the percentage of m/m mice. Data are presented as the mean ± S.D. and analyzed via a one-way ANOVA test followed by post-hoc Tukey’s multiple comparison tests. # p < 0.05, ## p < 0.01 and ### p < 0.001 vs. vehicle-treated m/m mice; * p < 0.05, ** p < 0.01 and *** p < 0.001 vs. vehicle-treated db/db mice.

Fig 3: LY294002 (a PI3K inhibitor) inhibited the phosphorylation of PI3K, AKT, and VEGFR2 in follicle microvascular endothelial-like cells of chicken (FMECs) induced by Angelica sinensis (AS) extract. ß-actin was used as an internal reference protein. All experiments were performed in triplicate, and the data are the mean ± S.E.M (*P < 0.05, **P < 0.01, ***P < 0.001).

Fig 4: Effects of Angelica sinensis (AS) extract on mRNA expression in follicle microvascular endothelial-like cells of chicken (FMECs) and granulosa cells (GCs). (A) Relative mRNA expression of PI3K, AKT, and VEGFR2 in FMECs. (B) Relative mRNA expression of PI3K, AKT, HIF1-a, and VEGF-A in GCs. All experiments were performed in triplicate, and the data are the mean ± S.E.M (*P < 0.05, **P < 0.01, ***P < 0.001).

Fig 5: Schematic diagram of the mechanism by which WAC improves NAFLD. WAC activates PI3K/AKT pathway, activates AMPK to promote SREBP-1c expression, thereby reducing hepatic TG synthesis and lipid synthesis.