Inhibition of Zn(PMFPCl) 2 on HepG2 cells and its mechanism
- VernacularTitle:Zn(PMFPCl)2对肝癌HepG2细胞的抑制作用及其机制
- Author:
Chengliang ZHAO
;
Youxin SONG
;
Long ZHAO
;
Sixi ZHANG
;
Liantai LI
- Publication Type:Journal Article
- Keywords:
Zn(PMFPCl) 2;
HepG2 cells;
proliferation;
cell cycle;
apoptosis-regulated proteins
- From:
Chinese Journal of Biochemical Pharmaceutics
2015;35(10):11-14
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the inhibition of Zn(PMFPCl) 2 on HepG2 cells and its mechanism.Methods The HepG2 cells were divided into control group and experimental group of 10, 30 and 70 μmol/L.The cell proliferation was detected by MTT assay, cell apoptosis and cell cycle was analysed by flow cytometry, cellular morphological change was observed with inverted microscope and the expressions of apoptosis-regulated proteins of p53, p21, caspase-3, bax and bcl-2 in HepG2 cells were detected by Western blot.Results The inhibitory rates of experimental groups (10, 30, 70μmol/L) at 24, 48 and 72h were significantly higher than those of control group (P<0.05), and the highest one was 63.29% of 70 μmol/L Zn (PMFPCl)2at 72 h.The apoptosis rates of each experimental group at 48h was significantly higher than that of control group (P<0.05).The cells were induced a remarkable G1 arrest by Zn(PMFPCl) 2 which could inhibit proliferation.The number of adherent cells reduced and cells shrank, convex on cytomembrane surface appeared and the cells changed to round and were brighter.Western blot results showed that the protein levels of p53, p21, caspase-3 and bax increased and bcl-2 decreased with the Zn(PMFPCl)2concentration increasing (P<0.05).Conclusion Zn(PMFPCl)2 could inhibit the proliferation and promote apoptosis of HepG2 cells whose mechanisms are promotation of p53, p21, caspase-3 and bax expressions and inhibition of bcl-2 expression.
