| Objectives: Silibinin is a traditional liver protect drug with high security. Inrecent years, it’s anti-cancer effects and multiple cancer chemoprevention has beendiscoveryed，but the influence on hypoxia HepG2cells is not clear, the present studyuse silibinin in cobalt chloride(CoCl2) induced hypoxia in HepG2cells, investigateimplications of silibinin on proliferation and apoptosis of hypoxia HepG2cells andit’s mechanisms to provide experimental data of silibinin targeted at applications ofhypoxic liver cancer cells in the clinical aspects.Methods: HepG2cells were cultured in vitro. To add different concentrations ofsilibinin while cobalt chloride induced hypoxia. Cell proliferation inhibition rate wasdetected by MTT assay. Cell apoptosis was observed by DAPI fluorescent staining,cell colony formation assay to observe the effects on cell proliferation, the cell cycleand apoptosis were detected by flow cytometry, and the expression of protein ofHIF-1α,Bcl-2was determined by Western-Blot assay.Results: MTT showed that silibinin has inhibited proliferation ability to hypoxicHepG2cells in a time and concentration dependent. Fluorescent staining showed thatwith increasing of drug concentration apoptosis increased.Colony formation assayshowed that with increasing of drug concentration cell colony reduced. Flowcytometry to test cell cycle shows that proportion of G1and G2phase decreased withincreasing concentration, hypoxic HepG2cells were arrested in S phase,andincreasing of silibinin’s concentration hypoxia HepG2cells apoptosisincreased.Western Blot display with the drug concentration increased, the expressionof protein of HIF-1α, Bcl-2has decreased in hypoxic HepG2cells. Conclusions:1. Silibinin could inhibitory the proliferation of hypoxia HepG2cells and induceapoptosis in hypoxia HepG2cells;2. Silibinin has possible effect on inducing the apoptosis and suppressionproliferation of hypoxic HepG2cells by decreasing the expression of HIF-1α, Bcl-2protein. |
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