Regulatory Role of GSK-3β on NF-κB, Nitric Oxide, and TNF-α in Group A Streptococcal Infection
Figure 3
Inhibition of GSK-3β downregulates NF-κB nuclear translocation and proinflammatory cytokine TNF-α production in macrophages after stimulation by NZ131. (a) Immunocytochemical staining for NF-κB p65 and DAPI for nuclear staining were used to determine the nuclear translocation of NF-κB in RAW 264.7 cells (2 × 105 cells/well in 24-well culture plate) 3 h after NZ131 infection (MOI: 10). Representative fields of NF-κB translocation in RAW 264.7 cells are shown. (b) The bar chart graph is the summary of (a) for the ratio of the change of NF-κB nuclear translocation after NZ131 infection and pretreatment with various GSK-3β inhibitors (LiCl, SB2, SB4, and BIO). The data for each treated or untreated group is the average result calculated by six randomly selected fields in one experiment. ((c) and (d)) The concentrations of TNF-α in RAW 264.7 cell culture supernatant 24 h after NZ131 stimulation and pretreatment with NF-κB inhibitor (PDTC) or GSK-3β inhibitor (BIO) were determined.
