BaoChun Wang1, Jian Xu2, HaiYang Wang3, ShunWu Chang1, Ning Liu1. 1. Department of General Surgery, Hainan Province People's hospital, 570311, China. 2. The department of Hepatopancreatobiliary Surgery, The 2nd Affliated Hospital of Hainan Medical University, 570000, China. Electronic address: xujian2017@hotmail.com. 3. Department of general surgery, The first hospital of Handan City, Hebei Province,056002, China.
Abstract
AIM: The aim of this study is to explain effect and mechanism of Sophoridine to suppress Hepatocellular carcinoma in vitro and vivo. METHODS: In vitro experiment, the HepG2 cells were divided into 5 groups: 0μg/mL Sophoridine treated group (0 μg/mL group); 10μg/mL matrine treated group (10μg/mL group); 20μg/mL matrine treated group (20μg/mL group) and 10μg/mL Paclitaxel treated group (Positive drug group). Measuring the cell proliferation of difference groups by MTS assay; evaluating cell apoptosis of difference by flow cytometry; the cell invasion and migration abilities of difference HepG2 cells were measured by transwell and wound healing testing; measuring the relative proteins expression in difference groups. In vovo experiment, the nude mice were divided into 5 groups: 0μg/mL, 5μg/mL, 10μg/mL, 20μg/mL and Positive drug groups, after executing, taking the tumor tissue from nude mice of difference groups, measuring the tumor volume and weight; evaluating the PTEN protein expression in tumor tissue by Immunohistochemistry (IHC). RESULTS: In the cell experiments, Compared with 0μg/mL group, cell proliferation rates were significantly reduced, cell aopotosis were significantly increased and invasion and wound healing abilities were significantly decreased in marine treated groups with dose-dependent (P<0.05, respectively). In the nude mice experiment, the tumor volume and weight of matrine treated groups were significantly decreased compared with 0 μg/mL group with dose-dependent (P<0.05, respectively). And the PTEN protein expression of Sophoridine treated groups were significantly decreased compared with 0μg/mL group with dose-dependent (P<0.05, respectively). CONCLUSION: Sophoridine had anti-cance effects to suppress HepG2 activities by regulation PTEN/PI3K/AKT, Caspase-3/-9 and MMP-2/-9 signaling pathway.
AIM: The aim of this study is to explain effect and mechanism of Sophoridine to suppress Hepatocellular carcinoma in vitro and vivo. METHODS: In vitro experiment, the HepG2 cells were divided into 5 groups: 0μg/mL Sophoridine treated group (0 μg/mL group); 10μg/mL matrine treated group (10μg/mL group); 20μg/mL matrine treated group (20μg/mL group) and 10μg/mL Paclitaxel treated group (Positive drug group). Measuring the cell proliferation of difference groups by MTS assay; evaluating cell apoptosis of difference by flow cytometry; the cell invasion and migration abilities of difference HepG2 cells were measured by transwell and wound healing testing; measuring the relative proteins expression in difference groups. In vovo experiment, the nude mice were divided into 5 groups: 0μg/mL, 5μg/mL, 10μg/mL, 20μg/mL and Positive drug groups, after executing, taking the tumor tissue from nude mice of difference groups, measuring the tumor volume and weight; evaluating the PTEN protein expression in tumor tissue by Immunohistochemistry (IHC). RESULTS: In the cell experiments, Compared with 0μg/mL group, cell proliferation rates were significantly reduced, cell aopotosis were significantly increased and invasion and wound healing abilities were significantly decreased in marine treated groups with dose-dependent (P<0.05, respectively). In the nude mice experiment, the tumor volume and weight of matrine treated groups were significantly decreased compared with 0 μg/mL group with dose-dependent (P<0.05, respectively). And the PTEN protein expression of Sophoridine treated groups were significantly decreased compared with 0μg/mL group with dose-dependent (P<0.05, respectively). CONCLUSION:Sophoridine had anti-cance effects to suppress HepG2 activities by regulation PTEN/PI3K/AKT, Caspase-3/-9 and MMP-2/-9 signaling pathway.