Fig 1: Effect of CIAA on the expression of AFP and AKT in HCC mice. (a) AFP protein expression and distribution in live tissue (scale bar = 100 µm); (b) AFP and AKT pathway protein expression in the liver tissue; (c) protein level relative expression of the western blot (data were presented as the mean ± standard deviation. ***p < 0.001 < 0.001, normalized to ß-actin); (d) AFP mRNA expression in the liver tissue (control vs. HCC, P < 0.001; HCC vs. CIAA, P < 0.01; control vs. CIAA, P < 0.001).
Fig 2: The expression of Akt of CMT-93 cells and CMT-93 PM by ELISA. CMT-93 and CMT-93 PM (1×106/sample) were serum starved overnight and incubated with SP-D (10 µg/ml) for 2 hours at 37°C. The cell lysate was prepared and the expression of Akt was calculated by ELISA using the Akt (pS473) + total Akt ELISA kits. CMT-93PM showed a relatively small change in Akt level due to the SP-D treatment compared to CMT-93 (0.20 vs. 0.11; P=0.10) (0.24 vs. 0.18, P=0.88). SP-D, surfactant protein D; CMT-93 PM, CMT-93 pulmonary metastases.
Fig 3: Effect of STGPT (20, 40 and 80 mg/kg) on p-AKT (ser473)/AKT (A); and FOXO3 mRNA (B) in mice with NDEA-induced HCC. Data are presented as the mean ± SD (n = 6). ++ p < 0.01 vs. Control group, +++ p < 0.001 vs. Control group, ++++ p < 0.vs.vs Control group, ***p < 0.vs. NDEA group, ****p < 0.0001 vs. NDEA group, #### p < 0.vs. STGPT 20 group, @@@@ p < 0.0001 vs. STGPT 40 group. Control, normal control group received the vehicle; STGPT 80, normal group received sitagliptin (80 mg/kg); NDEA, NDEA-induced HCC group received the vehicle; NDEA + STGPT 20, NDEA-induced HCC group treated with sitagliptin (20 mg/kg); NDEA + STGPT 40, NDEA-induced HCC group treated with sitagliptin (40 mg/kg); NDEA + STGPT 80, NDEA-induced HCC group treated with sitagliptin (80 mg/kg).
Fig 4: The expression of PI3KCA (A), PI3KR1 (B) and PTEN (C) was measured using qPCR in the control group, PMO group, PMO+Exos group and exosome group. (D) The expression of p-AKT (Thr308), p-AKT (Ser 473) and total-AKT were detected using western blotting in the control group, PMO group, PMO+Exos group and exosome group. The results of p-AKT (Thr308) (E), p-AKT (Ser 473) (F) were calculated using Image J software.
Fig 5: Weight gain and metabolic parameters of WT and AdipoQ-mCAT TG mice under physiological diet conditions (A). Percentage weight change over time from baseline (B). Plasma triglyceride levels (C). Fasting plasma glucose levels (D,E). Area under the curve analysis of IP-glucose tolerance test (F,G). Area under the curve analysis of IP-insulin tolerance test (H). Phosphorylated AKT/Total AKT ratio displayed as a percentage of vehicle control in insulin-stimulated adipose tissue. For statistical analysis, 2-way ANOVA was performed in (A); Mann–Whitney test was performed in (E,G); unpaired t-test was performed on (B,C,H). Normality was assessed using the Shapiro–Wilk test. All values are represented as means with error bars representing SEM. * p < 0.05, ** p < 0.01, *** p < 0.001.
Supplier Page from Abcam for Akt (pS473) + total Akt ELISA Kit