The cytoprotective effect of Rumex Aquaticus Herba extract against hydrogen peroxide-induced oxidative stress in AGS cells.

The Rumex Aquaticus Herba extract containing quercetin-3-ß-D-glucuronopyranoside (ECQ) has been reported to exhibit various pharmacological activities, including anti-inflammatory and anti-oxidative effects. This plant has been traditionally used for the treatment of diarrhea, disinfestation, edema and jaundice, and as an antipyretic drug. The aim of the present study was to investigate the ability of ECQ to protect against oxidative damage and to determine its signaling mechanism in AGS cells. The protein expressions of heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2) were measured by Western blots. Cell viability was measured by MTT assay. Intracellular reactive oxygen species (ROS) levels were measured using 2',7'-dichlorofluorescein diacetate. Glutathione peroxidase levels were measured using kits. The protein expressions of HO-1 and its upstream mediator, Nrf2, increased after ECQ treatment. The HO-1 inhibitor, ZnPP, repressed the protective effect of ECQ on H2O2-induced cell damage. We found that LY294002, a specific PI3 K/Akt inhibitor, suppressed ECQ-induced HO-1 expression. ECQ significantly attenuated H2O2-induced cytotoxicity and ROS generation. Also, ECQ enhanced the antioxidant enzyme activities of glutathione peroxidase. These results suggest that ECQ exerts a cytoprotective effect against H2O2-induced oxidative stress by upregulation of Nrf2/HO-1 via the PI3 K/Akt pathway.

Effect of ECQ on Iodoacetamide-Induced Chronic Gastritis in Rats.

This study investigated effect of extract containing quercetin-3-O-ß-D-glucuronopyranoside from Rumex Aquaticus Herba (ECQ) against chronic gastritis in rats. To produce chronic gastritis, the animals received a daily intra-gastric administration of 0.1 ml of 0.15% iodoacetamide (IA) solution for 7 days. Daily exposure of the gastric mucosa to IA induced both gastric lesions and significant reductions of body weight and food and water intake. These reductions recovered with treatment with ECQ for 7 days. ECQ significantly inhibited the elevation of the malondialdehyde levels and myeloperoxidase activity, which were used as indices of lipid peroxidation and neutrophil infiltration. ECQ recovered the level of glutathione, activity of superoxide dismutase (SOD), and expression of SOD-2. The increased levels of total NO concentration and iNOS expression in the IA-induced chronic gastritis were significantly reduced by treatment with ECQ. These results suggest that the ECQ has a therapeutic effect on chronic gastritis in rats by inhibitory actions on neutrophil infiltration, lipid peroxidation and various steps of reactive oxygen species (ROS) generation.

Changes in the Contents of Prosapogenin in the Red Ginseng (Panax ginseng) Depending on Steaming Batches.

This study compared the contents of ginsenosides depending on steaming conditions of red ginsengs to provide basic information for developing functional foods using red ginsengs. The red ginseng steamed eight times at 98℃ ranked atop the amounts of prosapogenins ever detected in red ginsengs (ginsenoside Rg2, Rg3, Rg5, Rg6, Rh1, Rh4, Rk1, Rk3, F1, F4, 1.15%) among red ginsengs steamed more than twice. When steamed eight times at 98℃, 2.7 times as much prosapogenins such as ginsenosides Rg2, Rg3, Rg5, Rg6, Rh1, Rh4, Rk1, Rk3, F1, and F4 as those steamed just once at 98℃ was collected. In addition, the red ginsengs steamed eight times at 98℃ contained more amounting ginsenoside Rg3 (0.28%) than that in the red ginseng steamed several times at random. Accordingly, it is recommendable that red ginsengs steamed 8 times, which proved to be the optimal steaming condition, be used rather than those steamed 9 times (black ginsengs), in order to develop red ginseng products of high prosapogenin concentration and high functions.

The effect of quercetin-3-O-ß-D-glucuronopyranoside on indomethacin-induced gastric damage in rats via induction of mucus secretion and down-regulation of ICAM-1 expression.

The mechanism of the protective effect of quercetin-3-O-ß-D-glucuronopyranoside (QGC) from the leaves of Rumex aqauticus on indomethacin (IND, a representative NSAID)-induced gastric damage in rats was investigated. Pre-treatment with QGC significantly attenuated IND-induced gastric mucosal injury. An increase in myeloperoxidase (MPO) activity and expression of intercellular adhesion molecule (ICAM)-1 protein and mRNA expression of the pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1ß, as well as a decrease in gastric mucus secretion were detected in the gastric mucosa of IND-treated rats. QGC reversed the side effect of IND on MPO activity and mucus production. Furthermore, QGC pre-treatment notably decreased ICAM-1 protein and mRNA expression of the pro-inflammatory cytokines, suggesting that QGC protection from IND-induced damage is associated with increased gastric mucus secretion, inhibition of free radical production by activated neutrophils via ICAM-1, and pro-inflammatory cytokine downregulation.

Inhibitory effects of diterpene acids from root of Aralia cordata on IgE-mediated asthma in guinea pigs.

This study evaluated the anti-asthmatic activities of four diterpene acids isolated from Aralia cordata root that are proposed to be the active ingredients in its traditional use as a treatment for inflammation, overheating, pain and spasm in Korea. The diterpene acids were identified as kaurenoic acid, 7-oxo-sandaracopimaric acid, 17-hydroxy-ent-kaur-15-en-19-oic acid, and hederagenin, by comparing their phytochemical and spectroscopic data with previous reports. The effects of diterpene acids on asthma were evaluated by determining the specific airway resistance (sRaw) during the immediate asthmatic response (IAR) and the late-phase asthmatic response (LAR) in guinea pigs with IgE-mediated asthma. Recruitment of leukocytes and the presence of chemical mediators in bronchoalveolar lavage fluid (BALF) were determined, and histopathological surveys performed. The four diterpene acids dosed at 25 approximately 100 mg/kg had dose-dependently anti-asthmatic effects: 7-oxo-sandaracopimaric acid > 17-hydroxy-ent-kaur-15-en-19-oic acid > kaurenoic acid > hederagenin. 7-oxo-sandaracopimaric acid (25 mg/kg) significantly (p < 0.05) inhibited sRaw by 59.5% in IAR and LAR, and also dose-dependently inhibited recruitment of eosinophils and neutrophils into lung and release of chemical mediators, histamine, and the activity of phospholipase A(2) and eosinophil peroxidase in BALF. 7-Oxo-sandaracopimaric acid had the highest activity among the diterpene acids. But its effect was lower than cromolyn sodium, salbutamol, or dexamethasone in both the IAR and the LAR. These results suggested that C(7)-oxo radical of 7-oxo-sandaracopimaric acid was more active than the C(7)-hydroxy and hydrogen of the other compounds, and showed diterpene acids have anti-asthmatic effects, supporting the traditional application of this herb in treating IgE-mediated asthma.

The Inhibitory Effect of Quercetin-3-O-beta-D-Glucuronopyranoside on Gastritis and Reflux Esophagitis in Rats.

It was evaluated the inhibitory action of quercetin-3-O-beta-D-glucuronopyranoside (QGC) on reflux esophagitis and gastritis in rats. QGC was isolated from the herba of Rumex Aquaticus. Reflux esophagitis or gastritis was induced surgically or by administering indomethacin, respectively. Oral QGC decreased ulcer index, injury area, gastric volume, and acid output and increased gastric pH as compared with quercetin. Furthermore, QGC significantly decreased gastric lesion sizes induced by exposing the gastric mucosa to indomethacin. Malondialdehyde levels were found to increase significantly after inducing reflux esophagitis, and were reduced by QGC, but not by quercetin or omeprazole. These results show that QGC can inhibit reflux esophagitis and gastritis in rats.

The signaling mechanism of the sphingosylphosphorylcholine-induced contraction in cat esophageal smooth muscle cells.

We investigated the signaling pathway on sphingosinephosphorylcholine (SPC) -induced contraction in cat esophageal smooth muscle cells. SPC induced in a dose-dependent manner contractile effect. We have previously shown that lysophospholipid (LPL) receptor subtypes including the S1P1, S1P2, S1P3, and S1P5 receptor are present in esophageal smooth muscle. Only EDG-5 (S1P2) receptor antibody penetration into permeablilized cells inhibited the SPC-induced contraction. Pertussis toxin (PTX) and specific antibodies to G(i1), G(i2), G(i3) and G(o) inhibited the contraction, implying that SPC-induced contraction depends on PTX-sensitive G(i1), G(i2), G(i3), and G(o) protein. A phospholipase inhibitor U73122 and incubation of permeabilized cells with PLC-beta3 antibody inhibited SPC-induced contraction. The PKC-mediated contraction may be isozyme specific since only PKCepsilon antibody inhibited the contraction. Preincubation with MEK inhibitor PD98059 blocked the SPC-induced contraction, but p38 MAPK inhibitor SB202190 did not. Cotreatment with GF109203X and PD98059 did not show synergistic effects, suggesting that these two kinases are involved in the same signaling pathway in the SPC-induced contraction. The data suggest that S1P-induced contraction in feline esophageal smooth muscle cells depends on activation of the G(i1), G(i2), G(i3) and G(o) proteins and the PLCbeta3 isozyme via the S1P2 receptor, leading to stimulation of a PKCE pathway, which subsequently activates a p44/p42 MAPK pathway.

The effect of luteolin-7-O-beta-D-glucuronopyranoside on gastritis and esophagitis in rats.

This study evaluated the inhibitory action of luteolin-7-O-beta-D-glucuronopyranoside, luteolin which was isolated from Salix gilgiana leaves, and omeprazole on reflux esophagitis and gastritis in rats. Reflux esophagitis and gastritis were induced surgically and by the administration of indomethacin, respectively. The intraduodenal administration of luteolin-7-O-beta-D-glucuronopyranoside decreased the ulcer index, injury area, gastric volume and acid output, and increased the gastric pH compared with luteolin. Luteolin-7-O-beta-D-glucuronopyranoside significantly decreased the size of the gastric lesions that had been induced by exposing the gastric mucosa to indomethacin. The malondialdehyde content, which is the end product of lipid peroxidation, was increased significantly after inducing of reflux esophagitis. The malondialdehyde content was decreased by Luteolin-7-O-beta-D-glucuronopyranoside but not luteolin or omeprazole. Luteolin-7-O-beta-D-glucuronopyranoside has a more potent antioxidative effect than luteolin. Luteolin-7-O-beta-D-glucuronopyranoside is a promising drug for the treatment of reflux esophagitis and gastritis.

Metabolomic differentiation of deer antlers of various origins by 1H NMR spectrometry and principal components analysis.

The metabolomic analysis of various types of deer antler was performed by 1H NMR spectrometry and principal components analysis (PCA). The PCA of the 1H NMR spectra of the aqueous fractions allowed a clear discrimination between antler samples according to their origins by the first three principal components (PC1, PC2, and PC3), which cumulatively accounted for 93.5% of the variation in all variables. In particular, the score plots by the combination of PC1 and PC3 allowed an excellent separation of the antler samples. In addition, the major peaks in 1H NMR spectra contributing to the discrimination were assigned to lactate, alanine, acetic acid, choline, glycine, valine, tyrosine, and phenylalanine. This metabolomic-analysis-based method allows various types of deer antler to be efficiently differentiated without any pre-purification steps.

Studies on the anti-inflammatory effects of Clerodendron trichotomum Thunberg leaves.

Clerodendron trichotomum Thunberg Leaves (CTL) have been used for centuries in Chinese folk medicine for their anti-inflammatory properties. We have studied the anti-inflammatory effects of CTL extracts in rats, mice and in Raw 264.7 cells. 1 mg/kg solutions of the 30% and 60% methanol extracts of CTL were used and a 1 mg/kg of indomethacin was used as a positive anti-inflammatory standard; these were then administrated to rats. Carrageenan was injected subcutaneously to induce hind paw edema in rats. The result of carrageenan-induced rat paw oedema showed that a 1 mg/kg of the 30%, and 60% methanol fraction of CTL and 1 mg/kg of indomethacin inhibited the hind paw edema by 19.5%, 23.0%, and 20.5% respectively. The effect of CTL on inflammation in mice by a capillary permeability assay was examined by detecting Evans blue leakage from capillaries after the intraperitoneal injection of acetic acid, a potent inflammatory stimulus. The 60% methanol fraction of CTL inhibited Evans blue dye leakage by 47.0%, which was 10% higher than that of the inhibition of 1 mg/kg of indomethacin. Also, the 60% methanol fraction of CTL suppressed the prostaglandin E2 (PGE2) generation in RAW 264.7 macrophage cells after treatment with lipopolysaccharide (LPS) by as much as the inhibition of 1 mg/kg of indomethacin and this led to the synthesis of PGE2 by COX-2 induction. The inhibition of the carrageenan-induced rat paw oedema, vascular permeability and the PGE2 generation demonstrates that the 60% methanol fraction of CTL contains a potent anti-inflammatory activity.

Activity-guided isolation of saponins from Kalopanax pictus with anti-inflammatory activity.

By bioassay-guided separation, a known saponin, kalopanaxsaponin A (1) and a new saponin, pictoside A (2) were isolated from the stem bark of Kalopanax pictus as anti-inflammatory components when evaluated by vascular permeability test. Another novel saponin, pictoside B (3) was also isolated but was inactive in the test system used. The structures of pictosides A and B were elucidated as caulophyllogenin 3-O-alpha-L-rhamnopyranosyl(1-->2)-alpha-L-arabinopyranoside (2) and pictogenin (3beta,6beta,16alpha,23-tetrahydroxyolean-12-ene-28-oic acid) 3-O-alpha-L-arabinopyranoside (3), respectively, by spectral analysis and by chemical degradation. Kalopanaxsaponin A and pictoside A showed significant anti-inflammatory activity at the oral doses of 50 mg/kg.