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 2

Inhibited TLR4/MyD88 and NF-κB activations 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 TLR4/MyD88 and NF-κB activations. CGA treatment significantly mitigated LPS-PG-induced TLR4/MyD88 and phosphorylation of p65, one subunit of NF-κB, stimulation in HGF-1 cells. The relative protein expression of each target was measured by densitometry and normalized to protein levels of actin, an internal control. 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; HGF: human gingival fibroblast; LPS-PG: lipopolysaccharide from P. gingivalis; MyD88: myeloid differentiation primary response gene 88; NF-κB: nuclear factor-κB; TLR4: Toll-like receptor 4.

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