The effects of JGL on acute topical inflammation were analyzed by using the xylene-induced mouse ear edema model, which is a simple and classic model for acute exudative inflammation with local vasodilation, increased capillary permeability, and inflammatory cell infiltration caused by the release of histamine, bradykinin, and other inflammatory mediators.38 The method was performed as described previously with some slight modification.39 Male mice were randomly divided into six groups with ≥9 mice in each group, which included normal control (treated with 0.5% CMC-Na), xylene model (treated with 0.5% CMC-Na), positive control (0.19 g/kg aspirin), and JGL at three different doses. All mice were orally gavaged once daily for 7 consecutive days. On Day 7, one hour after the treatment, inflammation was induced in mice (except for the normal control group) as ear edema by 20 μL of xylene smeared on both surfaces of the right ear, whereas the left ear was left untreated. After 30 min, the mice were sacrificed. The ears were collected using a biopsy punch with a diameter of 9 mm and weighed. Ear edema was defined as the difference in weight between the two ears.
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