Inhibition of trypsin-induced mast cell activation by acanthoic acid.

Acanthoic acid (AA) is a pimaradiene diterpene isolated from the Korean medicinal plant, Acanthopanax koreanum (Araliaceae). In the present study, we examined whether AA has the inhibitory effect on the production of inflammatory mediators and activating signals induced in trypsin-treated human leukemic mast cell-1 (HMC-1). HMC-1 cells were stimulated with trypsin (100 nM) in the presence or absence of AA (1, 10, and 100 microg/ml). We assessed the production of TNF-alpha and tryptase by enzyme-linked immunosorbent assay (ELISA) or reverse transcription-PCR, ERK activation by Western blot, and NF-kappaB activation by gel shift assay. AA (10 and 100 microg/ml) significantly inhibited production of both TNF-alpha and tryptase in a dose-dependent manner in trypsin-stimulated HMC-1. Furthermore, AA inhibited ERK phosphorylation and NF-kappaB activation induced by trypsin treatment without blocking of trypsin activity even with 100 microg/ml. These results suggest that AA may inhibit the production of inflammatory mediators through inhibition of ERK phosphorylation and NF-kappaB activation pathway in human mast cells. It supports the evidence that AA may be used to blocks the development of inflammation caused from mast cells.

Effect of processed Scutellaria baicalensis on dextran sulfate sodium-induced colitis in mice.

Scutellaria baicalensis Georgi (Labiatae) has been used in the treatment of inflammatory diseases. Drug processing (Poje) is the process of treating crude drugs by several methods before use. The aim of this study was to determine the effect of processed Scutellaria baicalensis on experimental ulcerative colitis induced by dextran sulfate sodium (DSS). The types of processed Scutellaria baicalensis used in this study were parched Scutellaria baicalensis (PS) and rice wine-baked Scutellaria baicalensis (RWBS). Experimental colitis was induced in mice using a daily treatment of 5% DSS in the drinking water for 7 days. The water extracts of processed Scutellaria baicalensis (1 g/kg) were administered orally once a day for 7 days. The mice were divided in four groups: i) water plus DSS group, ii) crude Scutellaria baicalensis (CS) plus DSS group, iii) PS plus DSS group, and iv) RWBS plus DSS group. RWBS ameliorated all of the inflammatory symptoms, such as body weight loss, rectal bleeding and histological damage, compared to CS. Furthermore, RWBS significantly reduced the mucosal myeloperoxidase activity, and TNF-alpha (tumor necrosis factor-alpha), COX-2 (cyclooxygenase-2), NF-kappaB (nuclear factor-kappa B) and chymase expression more than CS. But these effects were not shown in the PS plus DSS group. Efficacy of Scutellaria baicalensis was increased after rice wine baking, but not after parching. The findings in this study suggest that RWBS may be a useful therapeutic agent for ulcerative colitis.

Inhibition of trypsin-induced mast cell activation by water fraction of Lonicera japonica.

Lonicera japonica Thunb.(Caprifoliaceae) has long been known as an anti-inflammatory. In the present study, the effect of water fraction of Lonicera japonica (LJ) on trypsin-induced mast cell activation was examined. HMC-1 cells were stimulated with trypsin (100 nM) in the presence or absence of LJ (10, 100, and 1000 microg/mL). TNF-alpha and tryptase production were measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR. Extracellular signal-regulated kinase (ERK) phosphorylation was assessed by Western blot. Trypsin activity was measured by using Bz-DL-Arg-p-nitroanilide (BAPNA) as substrate. LJ (10, 100, and 1000 microg/mL) inhibited TNF-alpha secretion in a dose-dependent manner. LJ (10, 100, and 1000 microg/mL) also inhibited TNF-alpha and tryptase mRNA expression in trypsin-stimulated HMC-1. Furthermore, LJ inhibited trypsin-induced ERK phosphorylation. However, LJ did not affect the trypsin activity even 1000 microg/mL. These results indicate that LJ may inhibit trypsin-induced mast cell activation through the inhibition of ERK phosphorylation than the inhibition of trypsin activity.

Acanthoic acid inhibits IL-8 production via MAPKs and NF-kappaB in a TNF-alpha-stimulated human intestinal epithelial cell line.

BACKGROUND: Intestinal epithelial cells (IECs) can produce cytokines and chemokines that play an important role in the mucosal immune response. Regulation of this production is important to prevent inflammatory tissue damage. The root and stem barks of Acanthopanax species have been used as a tonic and sedative as well as in the treatment of rheumatism and diabetes. The aim of this study was to examine the inhibitory effect of acanthoic acid isolated from Acanthopanax koreanum (Araliaceae), on IL-8 production via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappaB) in TNF-alpha-stimulated human colon epithelial cells. METHODS: HT29 cells were stimulated with TNF-alpha in the presence or absence of acanthoic acid. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR (RT-PCR). MAPK activation and IkappaB/NF-kappaB expression were assessed by Western blot analysis. NF-kappaB activation was determined using immunofluorescence localization and electrophoretic mobility shift assay (EMSA). RESULTS: Acanthoic acid suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. Furthermore, acanthoic acid inhibited TNF-alpha-induced MAPKs (p38, JNK1/2, and ERK1/2) activation, IkappaB degradation, NF-kappaB nuclear translocation, and NF-kappaB/DNA binding activity. CONCLUSION: Acanthoic acid might inhibit TNF-alpha-mediated IL-8 production by blocking in both the MAPKs and NF-kappaB pathways in HT29 cells.

The aqueous extract of Solanum melongena inhibits PAR2 agonist-induced inflammation.

BACKGROUND: Solanum melongena L. (Solanaceae) has antioxidant, analgesic, hypolipidemic and antiallergic activity. METHODS: The anti-inflammatory effects of the water extract of the S. melongena (SMWE) were investigated in PAR2-mediated mouse paw edema. Paw edema was induced by injection of trypsin or trans-cinnamoyl-LIGRLO-NH(2) (tc-NH(2)) into the hindpaw of mice. The SMWE (1, 5, 10, and 100 mg/kg) was orally administered 1 h before induction of inflammation. RESULTS: At doses of 5, 10, and 100 mg/kg, the SMWE showed significant inhibition of both paw edema and vascular permeability. The SMWE (10 mg/kg) significantly also inhibited PAR2 agonist-induced myeloperoxidase (MPO) activity and tumor necrosis factor (TNF)-alpha expression in paw tissue. CONCLUSION: These results demonstrate that the SMWE inhibits PAR2 agonist-induced mouse paw edema.