Chlorogenic Acid as a Positive Regulator in LPS-PG-Induced Inflammation via TLR4/MyD88-Mediated NF-κB and PI3K/MAPK Signaling Cascades in Human Gingival Fibroblasts

Figure 3

Attenuated phosphorylation of Akt and ERK by CGA treatment in LPS-PG-stimulated HGF-1 cells. Cells were treated with the indicated concentrations CGA and LPS-PG (1 μg/mL) for 4 h at 37°C in a humidified atmosphere containing 5% CO₂ in order to analyze the phosphorylation of signaling molecules. CGA treatment inhibited LPS-PG-stimulated phosphorylation of Akt and ERK in HGF-1 cells. The relative protein expression of each target was measured by densitometry and normalized to protein levels of unphosphorylated forms of each signaling molecule. Data represent the of triplicate experiments. ^# vs. NC group; and vs. LPS-PG group. Negative control (NC) group refers that CGA and LPS-PG were not treated. CGA: chlorogenic acid; JNK: c-Jun N-terminal kinase; ERK: extracellular regulated kinase; HGF: human gingival fibroblast; LPS-PG: lipopolysaccharide from P. gingivalis.