Fig 2: Apatinib inhibited esophageal cancer growth via the Akt/ß-catenin pathway in vivo. a All xenograft models were sacrificed and photographed after treatment with vehicle or apatinib (10 and 30 mg/kg/day). n = 5 mice per group. b Tumor volume (expressed in mm3) of xenografts was monitored every 2 days. Day 1 represents the first day of apatinib treatment. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. c Tumors were weighed at the end of the experiment, and weight was expressed in gram. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. d The weight of the mouse was monitored every 2 days, and weight was expressed in gram. P values were determined by one-way ANOVA with Tukey’s correction. NS represents no significance. e Xenograft tumors in the indicated groups were detected by immunofluorescence. Representative images of CD31 (green) and nuclei staining (DAPI, blue). Scale bar, 100 µm. f PCNA staining in the indicated groups was detected by IHC. Scale bar, 100 µm. g Xenograft tumors in the indicated groups were detected by immunofluorescence. Representative images of TUNEL (green) and nuclei staining (DAPI, blue). Scale bar, 100 µm. h The mRNA expression levels of Myc and Jun in tumor samples from the indicated groups were examined by qPCR. Data represent experiments in three independent tumors. P values were determined by one-way ANOVA with Tukey’s correction. **P < 0.01. i The protein levels of p-VEGFR2, p-Akt, ß-catenin and CyclinD1 in tumor samples from the indicated groups were determined by western blotting

Fig 3: Capsaicin reduced hepatic progenitor cells (HPCs) activation, and induced HPCs apoptosis in the liver of diethylnitrosamine (DEN)-induced rats suffering from hepatocellular carcinoma. (A) Immunohistochemistry staining showed that the expression of HPCs markers, EpCAM, OV6, SOX9 as well as proliferation marker PCNA was decreased in the DEN+capsaicin group compared to the DEN group. (B) Tunnel staining showed a higher number of apoptotic cells in the DEN+capsaicin group than that in the DEN group. (C) Immunofluorescence co-staining of Caspase-3 and EpCAM suggested capsaicin-induced HPCs apoptosis in DEN-treated rat liver. Scale bars, 40 µm

Fig 4: ACOT7 facilitated proliferation in vivo. (A) The image of tumors and tumor volume of the nude mice subcutaneously injected with 1×107 ACOT7-SK-Hep1 cells or control SK-Hep1 cells. (B) Representative HE staining and expression of ACOT7, Ki67 and PCNA determined by IHC. Unpaired two-tailed Student’s t-test was adopted. All data are shown as the mean±SD. ***p<0.001.

Fig 5: Effects of the oral administration of P. pentosaceus SMM914 on the antioxidation capacity and activation of the cytoprotective Nrf2 pathway in piglets. (a) Experimental outline in piglets (n = 18). Piglets were kept for 10 days after birth for adaptation. Oral administration of P. pentosaceus SMM914 was performed on days 10, 12, 14, 16 and 18 at low or high doses. At day 7 postweaning, seven piglets per treatment were randomly selected for slaughter for sample collection. (b) Alanine amiotransferase (ALT) and lactate dehydrogenase (LDH) were significantly decreased in piglets administered P. pentosaceus SMM914. (c-d) A graph and a bar chart of western blotting showing Nrf2 protein expression levels in the liver normalized to PCNA expression in the nucleus. (e-f) Western blotting analysis of antioxidant protein (Keap1, NQO-1, HO-1, SOD1 and CAT) levels in the liver and bar graph of data showing their protein expression normalized to ß-actin expression in hepatic cells (n = 6). (g) The enzyme activities of GSH-Px, SOD, CAT and MDA were measured in liver lysates. Values of the bars stand for significant differences using one-way ANOVA followed by Duncan’s multiple comparisons at p <0.05. Data are the mean ± s.e.m, n = 7