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.
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.
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.
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.
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.
As compared to Bud, the equilibrium solubility of <b>3a</b>, <b>3c</b>, and <b>3e</b> was significantly increased; <b>3a</b>, <b>3b</b>, and <b>3c</b> significantly inhibited the interleukin-6 production in lipopolysaccharide-induced A549 cells; <b>3a</b> and <b>3e</b> could significantly decrease the xylene-induced ear edema; and <b>3a</b> and <b>3c</b> were gradually and slowly hydrolyzed into Bud in the alveolar fluid and lung homogenate and broken down quickly in plasma.
KOTMIN13 decrease the production of No, PGE<sub>2</sub>, and proinflammatory cytokine (TNF-∝, IL-1β,IL-6).KOTMIN13 Suppressed the degradation of NF-kβ and IKβα and the phosorylation of MAP Kinases.Topical application of KOTMIN13 reduced mouse ear edema.Oral administration of KOTMIN13 decreased carrageenan-induced paw edema.
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.
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 anti-inflammatory activity was investigated using the carrageenan, egg albumin, or histamine-induced rat paw edema as well as xylene-induced ear edema, capillary permeability, and cotton pellet granuloma while the antinociceptive activity was evaluated using the mouse writhing, formalin, and hot-plate tests.
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.
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.
The methanol extract and derived fractions were evaluated for anti-inflammatory activity by using in vitro heat induced albumin denaturation assay and various in vivo assays; carrageenan-induced hind paw edema method, Freunds' complete adjuvant induced arthritis, histamine induced paw edema and xylene induced ear edema in Sprague Dawley rat.
We concluded that AA plays a role in the development of TRPV3-mediated ear edema and that this result may contribute to better understanding of the pathophysiological mechanisms involved in the development of a certain type of edema.
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.
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.
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.
In two animal models, carrageenan-induced paw edema and phorbol ester-induced ear edema, PEA attenuates inflammation in wild-type mice but has no effect in mice deficient in PPAR-alpha.
In a murine model of arachidonic acid-induced ear inflammation, the LTA(4)H inhibitor, JNJ-26993135 (1-[4-(benzothiazol-2-yloxy)-benzyl]-piperidine-4-carboxylic acid), dose-dependently inhibited ex vivo LTB(4) production in blood, in parallel with dose-dependent inhibition of neutrophil influx (ED(50), 1-3 mg/kg) and ear edema.