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Cholesterol induces autophagic and apoptotic death in gastric carcinoma cells
Lim, S.-C.,Parajuli, K.R.,Duong, H.-Q.,Choi, J.E.,Han, S.I. Spandidos Publications 2014 International journal of oncology Vol.44 No.3
Despite conflicting results, there is evidence to suggest an inverse link between total body cholesterol levels and the risk of certain malignancies. Based on previous reports, this phenomenon appears to vary with cancer site, and, in particular, more consistent data on inverse relations was reported in the risk of gastric cancer. In the current study, the effect of cholesterol on gastric cancer cell viability was examined using an in vitro cell culture system. Addition of cholesterol in culture medium resulted in reduced viability and clonogenicity of SNU601, SNU638 and SNU216 gastric cancer cells by induction of both autophagic and apoptotic death. Transient inactivation of ERK1/2 was linked to reduction of cholesterol-mediated cell viability, and tumor necrosis factor-related apoptosis-inducing ligand receptor 2 (TRAIL-R2/DR5) was also involved in cell death signaling. In conclusion, these results imply that cholesterol can act as a signal regulator to modulate cell viability and that proper cellular cholesterol levels may be advantageous to suppress growth of gastric carcinomas.
Safety assessment of So-cheong-ryong-tang: Subchronic toxicity study in Crl:CD Sprague Dawley rats
LEE, MEE-YOUNG,SEO, CHANG-SEOB,CHA, SHIN-WOO,SHIN, HYEUN-KYOO Spandidos Publications 2014 MOLECULAR MEDICINE REPORTS Vol.9 No.6
<P>So-cheong-ryong-tang, an oriental herbal formula, is used in Korea for treating pulmonary disorders, including asthma, bronchitis and allergic diseases. The objective of the present study was to investigate the potential adverse effects, if any, of subchronic administration of So-cheong-ryong-tang aqueous extract (SCRT) in male and female rats. In the present study, 0, 1,000, 2,000 and 5,000 mg/kg/day of SCRT was administered to Crl:CD Sprague Dawley rats (10/gender/group) for 13 weeks via oral gavage. Administration of the SCRT did not result in any mortality. There were no clinical or ophthalmological signs, changes in urinalysis, body weight, food consumption, gross findings, hematology, serum biochemistry, organ weight or histopathology attributable to the administration of SCRT. Any alterations noted were incidental and consistent with those historically observed in the age and strain of rats used in the present study. Based on the results of the present study, the no observed adverse effect level for SCRT under the present experimental conditions was determined to be 5,000 mg/kg/day, the highest dose assessed, for both genders.</P>
Induced production of anti-etanercept antibody in collagen-induced arthritis
YI, HYOJU,KIM, JURYUN,JUNG, HYERIN,RIM, YERI ALICE,KIM, YOUNGKYUN,JUNG, SEUNG MIN,PARK, SUNG-HWAN,JU, JI HYEON Spandidos Publications 2014 MOLECULAR MEDICINE REPORTS Vol.9 No.6
<P>Etanercept is a widespread biological drug for the treatment of rheumatoid arthritis, which inhibits tumor necrosis factor-α (TNF-α). Recently, the presence of antibodies targeting TNF-α inhibitors such as infliximab and adalimumab, was reported. However, few reports have studied etanercept in a mouse model of arthritis. We investigated the induction of anti-etanercept antibody production, along with the antibody's potential interfering effects on the biological function of etanercept, in mice with collagen-induced arthritis (CIA). CIA mice received an intraperitoneal injection of etanercept (25, 100 or 400 ?g per mouse). The degree of inflammation and cartilage erosion was evaluated, and the number of osteoclasts in the ankle joints was assessed by TRAP staining. The level of pro-inflammatory cytokines in the serum was measured. To analyze the anti-osteoporotic effect of etanercept, microfocal computed tomography analyses of femurs and tibias were performed. Etanercept treatment decreased both the incidence and severity of arthritis in a dose-dependent manner, except for the highest dose of 400 ?g. The mice that were treated with 25 and 100 ?g etanercept showed an improvement in inflammation, cartilage damage, and even bone loss. However, mice treated with 400 ?g etanercept showed no significant improvement in any of the tested parameters. Using a customized enzyme-linked immunosorbent assay (ELISA), the presence of the anti-etanercept antibody was detected in the serum in this treatment-refractory group. The therapeutic effect of etanercept was reduced in the CIA mice that developed the anti-etanercept antibody. In conclusion, the production of an anti-etanercept antibody can be induced in CIA mice, and this antibody can considerably reduce the anti-arthritic and anti-osteoporotic effects of etanercept.</P>
Bioactive peptide from Pyropia yezoensis and its anti-inflammatory activities
LEE, HYUN-AH,KIM, IN-HYE,NAM, TAEK-JEONG Spandidos Publications 2015 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.36 No.6
<P>Pyropia yezoensis (P. yezoensis) is an important marine algae. Its high protein content serves as a good source of biologically active peptides. Potent inhibitory effects on the production of inflammatory mediators were observed in a bioactive peptide derived from P. yezoensis (peptide from P. yezoensis; PPY1), as demonstrated in lipopolysaccharide (LPS)-stimulated macrophages. The present study showed that peptide concentrations ranging from 250 to 1,000 ng/ml had no significant cytotoxicity in the cell viability assay when applied to the RAW 264.7 cells for 24 h. PPY1 completely inhibited LPS-stimulated nitric oxide (NO) release in a dose-dependent manner. Fluorescence intensity, corresponding to intracellular reactive oxygen species (ROS) produced by 10 ng/ml LPS-stimulated cells, significantly shifted, indicating that the peptide reduced the level of ROS. Furthermore, PPY1 exerted potent inhibitory activity to reduce the release of pro-inflammatory cytokines (inducible NO synthase, cyclo-oxygenase-2, interleukin-1 beta and tumor necrosis factor-a) in LPS-stimulated macrophages in a dose-dependent manner. These results also showed that the anti-inflammatory activity of PPY1 was associated with downregulation of extracellular signal-regulated kinase, protein 38, and c-jun NH2-terminal kinase phosphorylation in the mitogen-activated protein kinase pathways. In conclusion, PPY1 can have a significant role as an anti-inflammatory agent, with a potential for use in marine products.</P>
Jeong, H.-J.,Oh, H.-A.,Lee, B.-J.,Kim, H.-M. Spandidos Publications 2014 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.33 No.1
In this study, we investigated the effects of Naju Jjok (Polygonum tinctorium Lour., NJJ) on interleukin (IL)-32 and thymic stromal lymphopoietin (TSLP) levels associated with allergic rhinitis (AR). Using female BALB/c mice, we created an animal model of ovalbumin (OVA)-induced AR. Prior to the callenge with OVA, the mice were administered, either nasally or orally with NJJ. In addition, we also used the eosinophilic cells line, Eol-1, stimulated with granulocyte-macrophage colony-stimulation factor (GM-CSF). The mRNA and protein levels of inflammatory cytokines and markers [interleukin (IL)-32, IL-4, macrophage-inflammatory protein-2 (MIP-2), intercellular adhesion molecule-1 (ICAM-1), and cyclooxygenase-2 (COX-2)] were measured by RT-PCR and western blot analysis, respectively and serum levels were measured by ELISA. The increased levels of IL-32 in the mice with AR and in the stimulated eosinophilic cell line, Eol-1, were significantly reduced by NJJ. TSLP levels were also decreased following the oral administration of NJJ. Mice orally administered NJJ showed markedly alleviated clinical symptoms, such as a reduced number of nasal rubs, decreased spleen weight, decreased serum immunoglobulin E (IgE) levels and decreased serum histamine levels. The oral administration of NJJ significantly decreased the IL-4 levels, while increasing the interferon- levels in the spleen. The increased number of eosinophils and mast cells infiltrating the nasal mucosal tissue of the mice with AR were decreased following the oral administration of NJJ. NJJ effectively attenuated caspase-1 activity in the mice with AR and in the stimulated Eol-1 cells. The oral administration of NJJ significantly reduced the levels of inflammatory markers, such as MIP-2, ICAM-1 and COX-2. Furthermore, the intranasal administration of NJJ significantly reduced the early phase response to allergen exposure, such as nasal rubs, IgE production and histamine release, as well as the late phase responses, such as the expression of inflammatory markers. In conclusion, these data demonstrate that NJJ may play a regulatory role in nasal inflammation.