title: CTB glycoprotein (75kDa) inhibits IgE releasing, TNF-α and IL-6 expressed by bisphenol A in vivo and in vitro.
abstract: Cudrania tricuspidata Bureau (CTB) has been used to treat allergies and inflammatory disease as folk medicine in Korea. The objective of this study is to determine whether a glycoprotein isolated from CTB (75 kDa) has a preventive potential of allergic inflammation caused by bisphenol A (BPA) in BALB/c mice and RBL-2H3 cells. Production of immunoglobulin (Ig) E and releasing of β-hexosaminidase and histamine at treatment of CTB glycoprotein (5-10mg/kg, BW) were evaluated in mice serum. Activation of extracellular signal-regulated kinases (ERK) and p38 mitogen-activated protein kinase (MAPK), activator protein (AP)-1, expressions of pro-inflammatory cytokines, nitric oxide (NO) production and cyclooxygenase (COX)-2 were assessed in RBL-2H3 cells. In the results, CTB glycoprotein (10mg/kg, BW) inhibited the production of IgE and releasing of β-hexosaminidase and histamine. Also, the CTB glycoprotein (100 μg/ml) blocked phosphorylation of ERK1/2 and p38 MAPK, and the activation of AP-1, while it inhibited the NO production, activities of COX-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-6, but not IL-1β. Taken together, the results of this study indicated that the CTB glycoprotein modulates the expression of allergic inflammation-related factors via the suppression of MAPK/AP-1 activation.
authors.affiliation: Molecular Biochemistry Laboratory, Biotechnology Research Institute & Center for the Control of Animal Hazards Using Biotechnology (BK 21), Chonnam National University, Gwang-ju, 300 Yongbong-Dong 500-757, South Korea.
authors.forename: Jin
authors.initials: J
authors.lastname: Lee
authors.forename: Sei-Jung
authors.initials: SJ
authors.lastname: Lee
authors.forename: Kye-Taek
authors.initials: KT
authors.lastname: Lim
mesh_terms: D000818:Animals; D001559:Benzhydryl Compounds; D015153:Blotting, Western; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D016207:Cytokines / Q000378:metabolism; D052244:Endocrine Disruptors / Q000633:toxicity*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006023:Glycoproteins / Q000494:pharmacology*; D006596:Hexosaminidases / Q000378:metabolism; D006636:Histamine Release / Q000187:drug effects; D006967:Hypersensitivity / Q000517:prevention & control*; D007073:Immunoglobulin E / Q000378:metabolism*; D007249:Inflammation / Q000517:prevention & control*; D015850:Interleukin-6 / Q000096:biosynthesis*; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D029586:Moraceae / Q000737:chemistry*; D010636:Phenols / Q000037:antagonists & inhibitors* / Q000633:toxicity*; D060888:Real-Time Polymerase Chain Reaction; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D051546:Cyclooxygenase 2; D016207:Cytokines; D052244:Endocrine Disruptors; D006023:Glycoproteins; D006596:Hexosaminidases; D007073:Immunoglobulin E; D015850:Interleukin-6; D020928:Mitogen-Activated Protein Kinases; D010636:Phenols; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; C006780:bisphenol A; D000098826:Bisphenol A Compounds