Apoptosis Effect And Mechanism Of Yun Zhi Chloroform Extract On Hepatoma Carcinoma HepG-2Cells

Objective To discuss the apoptosis effect and mechanism of Yun Zhi chloroform extract on hepatoma carcinoma HepG-2cells.Methods HepG-2cells were treated with different concentration of Yun Zhi chloroform extract for various duration. MTT Assay methods were used to measure the suppressive rate of Yun Zhi chloroform extract on the hepatoma carcinoma HepG-2cells and HE staining methods were applied to observe the cell morphological changes. The impact of Yun Zhi chloroform extract on DNA fragment of hepatoma carcinoma HepG-2cells was monitored with DNA ladder method. And Western Blotting method was used to analysis the influencing of Yun Zhi chloroform extract on the expression of Bax. Bcl-2and Caspase-3in hepatoma carcinoma HepG-2cells.Results Yun Zhi chloroform extract can inhibit proliferation of hepatoma carcinoma HepG-2cells and the inhibition effects increased with the prolongation of time and the increasing of drug concentration. The inhibition rate was52.3%, closing to IC50when the drug concentration was200j.μmol/L and the action time was48h. HE staining results showed that, compared with the control group, hepatoma carcinoma HepG-2cells which was treated by Yun Zhi chloroform extract broadened cells interval, and lost its natural position with nuclear shrinkage, high stained and cell fragmentation. And the apoptosis degree was more serious with the increasing of duration and drug concentration. There was no DNA ladder for control group while ladder characteristic of apoptosis was found for the other groups and there was significant difference of dosage between them. Compared to the control group, the expression of Bcl-2, Bax and Caspase-3of medication group was significantly changed (P＜0.01) while the expression of Bcl-2decreased and the expression of Bax and Caspase-3increased.Conclusion Yun Zhi chloroform extract could induce the apoptosis of hepatoma carcinoma HepG-2cells and the action was related to dosage and duration. The mechanism of apoptosis effect was relevant to the down-regulation of Bcl-2expression and the up-regulation of Bax and caspase-3expression.