Fig 1: Chrysin induces the apoptosis of ESCC cells in vitro. (A)–(C) The indicated ESCC cells were treated with chrysin (10, 25, and 50 µmol/L) for 48 h, cell apoptosis was evaluated by FCM assay (values of mean ± SD as indicated) (A), caspase 3/7 activity (B), and the cleavage of PARP (C). (D)–(F) The indicated ESCC cells were treated with 50 µmol/L chrysin with and without 50 µmol/L Z-VAD-FMK pretreatment, respectively. Cell viability was measured by MTS assay (D). Apoptosis was evaluated by caspase 3/7 activity (E). The cleavage of PARP was measured by ELISA assay (F). *P < 0.05, **P < 0.01, ***P < 0.001. Error bars, mean ± SD of five independent experiments.
Fig 2: Chrysin suppresses the proliferation and promotes apoptosis of ESCC tumors in vivo. (A) Animals harbored the indicated ESCC tumors were treated different doses of chrysin (10, 25, and 50 mg/kg/day, p.o.). The growth curves and representative images of tumor were shown. (B)–(G) Cleaved PARP (B), cleaved caspase 3 (C), and pFAK Tyr397/FAK (D), pAKT Ser473/AKT (E), pPRAS40 Thr246/PRAS40 (F), or pRPS6 Ser235/236/RPS6 (G) ratio in the indicated tumors was evaluated using quantitative ELISA assay. (H) Histopathologic analyses of major organs, including heart, liver, spleen, or kidney from control and different doses of chrysin (10, 25, and 50 mg/kg/day, p.o.). Magnification, 3 mm as indicated. *P < 0.05; **P < 0.01; ***P < 0.001. Error bars, mean ± SD of five independent experiments.
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