A Laboratory Evaluation of Medicinal Herbs Used in China for the Treatment of Hand, Foot, and Mouth Disease
Figure 4
Inhibition of infection-induced IκBα degradation by HCT and MHB. (a, d) Determination of the time courses of IκBα degradation during EV71 and CVA16 infections. Vero cells were infected with EV71 (a) or CVA16 (d) at an MOI of 3 for indicated times. The cytoplasmic levels of IκBα proteins were determined by immunoblotting assay. At 10 hr PI, IκBα was significantly degraded implying the NF-κB activation. (b, c) HCT treatment blocks IκBα degradation induced by EV71 infection and TNFα treatment. Vero cells were infected with EV71 (b, MOI = 3) for 10 hr or treated with 1 ng/mL TNFα (c) for 20 min in presence or absence of HCT at indicated concentrations. IκBα degradation was detected by immunoblotting assay. (e, f) MHB treatment blocks IκBα degradation induced by CVA16 infection and TNFα treatment. Vero cells were infected with CVA16 (e, MOI = 3) for 10 hr or treated with 1 ng/mL TNFα (f) for 20 min in presence or absence of MHB at indicated concentrations. IκBα degradation was detected by immunoblotting assay. GAPDH was used as a loading control. The results are representative of two independent experiments. TNFα (+) at 3 ng/mL was used as a positive control for IκBα degradation.
