Fig 5.

PDTC inhibited HSV replication neither through its antioxidant activity nor by blocking the MAPK pathway. (A) PDTC attenuated HSV-2-induced ROS production. HEC-1-A cells were infected with HSV-2 (MOI = 1) in the presence or absence of NAC (1 mM), APO (50 μg/ml), or PDTC. ROS levels were determined 24 h p.i. as described in the text. a.u., arbitrary units. (B) Both NAC and APO showed no anti-HSV-2 activity. Cells were infected with HSV-2 (MOI = 1) in the presence or absence of PDTC (12.5 μg/ml), NAC (1 mM), or APO (50 μg/ml), and the gD expression levels were determined 24 h p.i. (C) Cells transfected with AP-1-luc reporter plasmid were treated with serial concentrations of PDTC, SB203580 (20 μM), or SP600125 (20 μM) before being mock infected or infected with HSV-2 (MOI = 1). The RLU were determined 24 h p.i. and are expressed as the percentage of the amount in the mock-infected cells. (D) Cells were either mock infected or infected with HSV-2 (MOI = 1) in the presence or absence of PDTC. JNK/p38 MAPK activation was determined 12 h p.i. via Western blot assay. Error bars show standard deviations.