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논문 기본 정보

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학술저널
저자정보
Kim Yeon-Yong (Cell & Matrix Research Institute Department of Pharmacology School of Medicine Kyungpook National University Daegu Korea) Lee Soyoung (Immunoregulatory Materials Research Center Korea Research Institute of Bioscience and Biotechnology Jeongeup Korea.) Kim Min-Jong (Cell & Matrix Research Institute Department of Pharmacology School of Medicine Kyungpook National University Daegu Korea) Rho Mun-Chual (Immunoregulatory Materials Research Center Korea Research Institute of Bioscience and Biotechnology Jeongeup Korea.) 장용현 (Department of Dermatology School of Medicine Kyungpook National University Kyungpook National University Hospital Daegu Korea.) Kim Sang-Hyun (Cell & Matrix Research Institute Department of Pharmacology School of Medicine Kyungpook National University Daegu Korea)
저널정보
대한천식알레르기학회(구 대한알레르기학회) Allergy, Asthma & Immunology Research Allergy, Asthma & Immunology Research Vol.15 No.2
발행연도
2023.3
수록면
214 - 230 (17page)
DOI
10.4168/aair.2023.15.2.214

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Purpose: Asthma is a complex, heterogeneous chronic inflammatory airway disease with multiple phenotypes. There has been a great progress in managing asthma, but there are still unmet needs for developing uncontrolled asthma treatments. The present study aimed to determine the effectiveness of oleanolic acid acetate (OAA) from Vigna angularis against allergic airway inflammation and the underlying mechanism of action with a focus on mast cells. Methods: To investigate the effect of OAA in allergic airway inflammation, we used the ovalbumin (OVA)-sensitized and challenged mice. To examine allergic airway inflammation associated with immune responses of mast cell activation in vitro, various types of mast cells were used. Systemic and cutaneous anaphylaxis models were used for mast cell-mediated hyper-responsiveness in vivo. Results: OAA reduced OVA-induced airway inflammatory responses such as bronchospasm, increase of immune cell infiltration and serum immunoglobulin E and G1 levels. Especially, OAA decreased the mast cell infiltration, and β-hexosaminidase release as a mast cell activation marker in the bronchoalveolar lavage fluid. OAA inhibited mast cell degranulation in mast cell line (RBL-2H3) and primary cells (rat peritoneal mast cell and mouse bone marrow-derived mast cell). Mechanistically, OAA suppressed intracellular signaling pathways including the phosphorylation of phospholipase Cγ and nuclear factor-κB, resulting from the suppression of intracellular calcium influx and pro-inflammatory cytokine expression. Further, oral administration of OAA attenuated mast cell-mediated systemic and cutaneous anaphylaxis. Conclusions: Our study showed that OAA can inhibit mast cell-mediated allergic reaction. Consequently, the application of OAA to mast cells for the allergic airway inflammation facilitate a new direction of treating allergic asthma.

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