Inhibitory Effects Of Ginsenoside Rb1on Abnormal Changes Of Proliferation And Apoptosis Caused By HSV-1in Human Glioma Cells

Objective:1To establish an Herpes simplex virus-1(HSV-1) infection model of human glioma cells(U251) in vitro and investigate the inhibitory effects of Ginsenoside Rbl(GRbl) on apoptosis caused by HSV-1in U251.2To investigate the inhibitory effects of GRb1on Neurotrophins expression in U251cells caused by HSV-1infection.Materials and methods:1U251cells were infected by HSV-1at a multiplicity of infection of5while HSV-1group, control group, GRbl group and GRbl+HSV-1group were set up. Inverted microscope was chosen to detect the morphologic changes. Cell proliferation was detected by MTT assay. Cells apoptosis was measured by flow cytometry with Guava Nexin(?)Reagent.2U251cells were infected by HSV-1(MOI=5) while GRbl (400μg/ml) group, GRbl+HSV-1(400μg/ml) group, control group and HSV-1group were set up. NGF and BDNF expression were measured by RT-PCR and Western blot.Results:1We found that in the400μg/mL GRbl and400μg/mL GRbl+HSV-1groups, MTT values were higher than control group at all times (P<0.05). In HSV-1group, cells started to merge at12h post-infection and increase at24h post-infection. Cytopathic effects (CPE) were observed at36h post-infection. In400μg/ml GRbl+HSV-1group, a few merges appeared at24h post-infection and increased at36h post-infection when most cells kept normal forms. Cell apoptosis indicated that apoptosis rate in400μg/ml GRb1+HSV-1group was lower than HSV-1group(P<0.05).2RT-PCR and Western blot:In400μg/ml GRbl+HSV-1group, NGF expression were decrease at the early stage of infection(P<0.05),while it were more than HSV-1group at the late stage of infection (P<0.05).While the level of BDNF mRNA at12to48hpi was not significantly different.Conclusions:1U251cells are permissive for HSV-1.2400μg/ml GRb1has nothing to do with apoptosis of normal U251cells, but it could inhibit abnormality of U251cells apoptosis caused by HSV-1infection.3400μg/ml GRb1could inhibit abnormal changes of NGF expression in early HSV-1infection.