Effect of Curculigo orchioides on reflux esophagitis by suppressing proinflammatory cytokines.

This study was performed to investigate effects of Curculigo orchioides rhizome (curculiginis rhizome) on acute reflux esophigitis (RE) in rats that are induced by pylorus and forestomach ligation operation. Proinflammatory cytokine, as well as tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6 were all assayed and the expression of TNF-α and COX2 analyzed by RT-PCR. The esophagic tissue damage of reflux esophagitis rat was increased compared to that of normal intact group. However, the esophagic damage percentage from the extract of curculiginis rhizoma (ECR) 600 mg/kg and ECR 300 mg/kg were significantly lower than that of the RE control group. Administration of α-tocopherol (30 mg/kg) and ECR (600 mg/kg, 300 mg/kg, and 150 mg/kg) had a significant effect on the gastric acid pH in rats with induced reflux esophagitis (p < 0.05). The treatment with ECR significantly reduced the production of cytokines TNF-α, IL-1ß and IL-6 levels compared to the model group (p < 0.05). The expression of TNF-α and COX2 in the intact esophageal mucosa was low while those of the RE control group were significantly higher due to an inflammatory reaction in the esophagus. Compare to the model group, treatment with α-tocopherol or ECR significantly inhibited the expression levels of COX2 and TNF-α in a dose-dependent manner. These results suggest that anti-inflammatory and protective effects of ECR could attenuate the severity of reflux esophagitis and prevent esophageal mucosal damage.

Effect of ß-glucan originated from Aureobasidium pullulans on asthma induced by ovalbumin in mouse.

The objective of this study is to detect the effect of beta-glucan derived from Aureobasidium pullulans SM-2001, a UV induced mutant of A. pullulans on the ovalbumin (OVA) induced allergic asthma. The test articles were orally administered to OVA-inducing asthmatic mice 4 days after sensitization for 13 days at 31.25, 62.5 or 125 mg/kg levels. Three days after the OVA sensitization, ten mice were selected per group based on body weight and were sacrificed three days after the OVA aerosol challenge. The changes on the body weight, lung weight, total leukocytes in peripheral blood and total cells in bronchoalveolar lavage fluid (BALF) were observed with changes on the lung histopathology and histomorphometry. The results were compared with dexamethasone (DEXA) 3 mg/kg intraperitoneally treated mice. The results showed increases of body weight after the OVA aerosol challenge, lung weight, total leukocytes and eosinophils in peripheral blood, total cell numbers, neutrophil and eosinophils in BALF were detected in the OVA control compared to sham control (non-OVA). However, these changes from asthmatic responses were significantly or dose-dependently decreased in the beta-glucan-dosing groups compared to those of the OVA control. Therefore, it is concluded that beta-glucan has favorable effects on asthmatic response induced by OVA. It was found that beta-glucan 125 mg/kg showed similar or slightly lower efficacy compared with DEXA 3 mg/kg.

Human lysyl-tRNA synthetase is secreted to trigger proinflammatory response.

Although aminoacyl-tRNA synthetases (ARSs) are essential for protein synthesis, they also function as regulators and signaling molecules in diverse biological processes. Here, we screened 11 different human ARSs to identify the enzyme that is secreted as a signaling molecule. Among them, we found that lysyl-tRNA synthetase (KRS) was secreted from intact human cells, and its secretion was induced by TNF-alpha. The secreted KRS bound to macrophages and peripheral blood mononuclear cells to enhance the TNF-alpha production and their migration. The mitogen-activated protein kinases, extracellular signal-regulated kinase and p38 mitogen-activated protein kinase, and Galphai were determined to be involved in the signal transduction triggered by KRS. All of these activities demonstrate that human KRS may work as a previously uncharacterized signaling molecule, inducing immune response through the activation of monocyte/macrophages.