The positive controls also prevented both ear edema and the increased of MPO activity by 100% and 42 ± 8% (HC-030031), 54 ± 6% and 80 ± 4% (SB-366791), 100% and 54 ± 5% (indomethacin), 100% and 80 ± 4% (dexamethasone in skin inflammation model induced by phenol) and 100% and 97 ± 3% (dexamethasone in inflammation model induced by croton oil), respectively.
Se-DMC and meloxicam decreased the ear edema formation and protected against the increase in myeloperoxidase activity in mice ear induced by croton oil.
<i>In vivo</i>, DF showed a significant inhibition of ear edema and myeloperoxidase (MPO) activity, with evident reduction of the leukocyte infiltration into tissue.
Their anti-inflammatory effects were assayed with an ear edema model using 12-O-tetradecanoylphorbol-13-acetate, while the activity of myeloperoxidase was determined to evaluate the index of leukocyte infiltration.
To the chronic ICD model, the TcE and dexamethasone (10 μg/ear) also reduced the ear edema (66 ± 6% and 70 ± 5%) and the MPO activity (58 ± 14% and 84 ± 4%); on the 9th day of the experiment.
The LEO topical application at concentrations of 0.25, 0.5, and 1 mg/ear reduced edema formation, myeloperoxidase (MPO) activity, and nitric oxide (NO) production in croton oil-induced ear edema model.
The products evaluated (3, 6, 8, 9 and 10) showed the lower values of relative leukocyte migration at 30 µM (0.14, 0.07, 0.10, 0.13 and 0.07, respectively), while in ear edema and myeloperoxidase activity methods, all the compounds reduced inflammation, only 4 and 16 yielded unsatisfactory results.
Similar results were found for dexamethasone 0.10 mg/ear (positive control), which showed inhibitions of ear edema and MPO activity of 100% and 65%, respectively.
Antiedematogenic and anti-inflammatory effects of S. buxifolia were obtained with concentrations of 0.3, 1 and 3%, with maximal inhibition in the concentration of 1% for gel containing CE (inhibitions of 100, 73±0.05 and 97±0.08% for croton oil- or UVB irradiation-induced ear edema and myeloperoxidase activity, respectively) and EtOAc fraction (inhibitions of 79±0.05, 73±0.05 and 89±0.04% for croton oil- or UVB irradiation-induced ear edema and myeloperoxidase activity, respectively).
These derivatives displayed significant anti-inflammatory activity in vivo, suppressing mouse ear edema induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) and inhibiting myeloperoxidase activity, an index of neutrophil infiltration.
Furthermore, inhibition of TRPV3 by natural osthole reversed the severity of inflammatory dorsal skin and ear edema in a dose-dependent manner and also decreased expression of inflammatory factors TNF-<i>α</i> and IL-6.
The extracts and phytochemicals from peels of <i>C. grandis</i> were prepared, and anti-inflammatory activities were carried out <i>in vivo</i> and <i>in vitro</i>, including inhibiting xylene-induced ear edema and carrageenan-induced paw edema in mice and the production of inflammatory cytokines (interleukin 1β, prostaglandin 2, and tumor-necrosis factor α) in lipopolysaccharide (LPS)-induced RAW 264.7 cells.
Furthermore, in a tetradecanoylphorbolacetate (TPA)-treated mouse model, AA and IA could effectively attenuate mouse ear edema and pathological damage and reduced levels of cytokines including iNOS, COX-2, TNF-α, and IL-1β.
An evaluation of P. acnes-induced ear edema in rat ear was conducted to compare the in vivo antibacterial and anti-inflammatory effect of CEN1HC-Br, the expression of IL-8, TNF-α, MMP-2 and TLR2 was evaluated by immunohistochemistry and real time-PCR.
Compound <b>5</b> inhibits in vitro the secretion of NO (IC<sub>50</sub> = 36.96 ± 1.06 μM), IL-6 (IC<sub>50</sub> = 73.71 ± 3.21 μM), and TNF-α (IC<sub>50</sub> = 73.20 ± 5.99 μM) in RAW (Murine macrophage cells) 264.7 macrophages, as well as the activation of NF-κB (40% at 150 μM) in RAW-blue macrophages, while compound <b>7</b> has been described that inhibit the in vivo TPA-induced ear edema, and the in vitro production of NO, and the PLA2 enzyme activity.
Furthermore, sacran significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced mouse ear edema and mRNA expression levels of cyclooxygenase (COX)-2 as well as pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6.
SF peptide alone effectively reduced both mice ear edema and the elevated levels of cyclooxygenase-2, interleukin-6 and -1beta, and tumor necrosis factor-alpha, showing similar anti-inflammatory effect to that of PEP-1-FK506BP.
Heat induced albumin denaturation assay and in vitro cell cultures was carried out for in vitro anti-inflammatory activity, while various in vivo assays like TPA induced ear edema, croton oil induced anus edema, formalin and carrageenan-induced hind paw edema was investigated in Sprague-Dawley rats.
The in vivo anti-inflammatory activity was evaluated using the model of TPA (12-O-tetradecanoylphorbol-13-acetate) induced ear edema, and the polymorphonuclear cell migration was evaluated by mieloperoxidase (MPO) and analyzed histologically.
An <i>in vivo</i> experiment of irritant contact dermatitis (ICD) in mice induced by TPA showed that NCEUG reduced significantly the ear edema in mice when compared to the EUG solution, as well as the leukocyte infiltration and IL-6 level, possibly due to better skin permeation and irritancy blockage.