Genistein Inhibits The Proliferation Of RPE Cells Exposed To Hypoxia

It is suggested that genistein suppressed the proliferation ofRPE cells on normal culture.But the effects and mechanism ofGenistein on the proliferation of RPE cells exposed to hypoxiaremains unclear.This study is to investigate the them. With thecontrol group, the RPE cells exposed to hypoxia was built up.Different concentration of Gen were added into the anoxic RPE cellswith the last concentration was seperately 25,50,100uM. MTTassay was used to evaluate the vital force(indicated by Value A).The growing conditions of the RPE cells in different phases wereanalyzed by flow cytometry. The expressions of the proliferatingcell nuclear antigen (PCNA), CyclinD1, extracellular signal-regulated kinases (ERKs), big mitogen-activated proteinkinases-1 (BMK1) c-Jun N-terminal kinase(JNK) and p38MAPKwere detected with Western blot. In contrast to the control group,the animation,cells in S phase,the expression of PCNA andCyclinD1 of anoxic RPE cells increased. The hypoxia induced theproliferation of the RPE cells. With Gen, the animation,cells in Sphase,the expression of PCNA and CyclinD1 decreased. Geninhibited the proliferation by G1/S and S/G2 arrest. With strongerGen, the animation,the expression of PCNA and CyclinD1 wasgradually reduced. In the meantime, the expression of p-ERK1/2was lessened when the RPE cells were exposed to hypoxia andwaxed when Gen was added into. However no changes of BMK1,c-jun and p38MAPK expression and phosphorylation occurred in allgroups. These results showed that the proliferation of RPE cellsexposed to hypoxia was enhanced. Genistein could inhibit theproliferation of anoxic RPE cells and it had dose-effect relationship.Gen educed the effect by activated the ERK1/2 pathway.