Results
1) clinical scores improved [LPS txg; 3.90 ± 0.20, WD-Hpt txg; 2.40 ± 0.37 (P<0.05)], 2) the number of inflammatory cells in AqH decreased [LPS txg; 8.65 ± 1.41 × 105 cells/mL, WD-Hpt txg; 3.83 ± 1.20 × 105 cells/mL (P<0.05)], 3) AqH protein concentration reduced [LPS txg; 36.65 ± 2.71 mg/mL, WD-Hpt txg; 28.73 ± 2.36 mg/mL (P<0.05)], and 4) decreased levels of TNF-α [LPS txg; 69.55 ± 7.38 pg/mL, WD-Hpt txg; 35.18 ± 9.22 pg/mL (P<0.001)], iNOS [LPS txg; 153.37 ± 12.72 μM, WD-Hpt txg; 110.79 ± 13.27 μM (P<0.05)], and COX-2 [LPS txg; 1,080.56 ± 196.06 pg/mL, WD-Hpt txg; 477.80 ± 66.61 pg/mL (P<0.01)] in AqH were observed, and histopathological grades improved [LPS txg; 2.80 ± 0.40, WD-Hpt txg; 1.50 ± 0.50 (P<0.05)]. Immunostaining and mRNA analysis revealed that 50 mg/kg WD-Hpt effectively suppressed iNOS, COX-2, NF-κB p65, IκB-α degradation, p-IKKα/β, β-catenin, and GSK-3β expression. These findings suggested that WD-Hpt exerts anti-inflammatory effects by targeting the NF-κB and Wnt/β-catenin pathways.