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Suppressive Effects of Ginsan on the Development of Allergic Reaction in Murine Asthmatic Model

Lim Y.-J.b, c · Na H.-S.a, b · Yun Y.-S.e · Choi I.S.d · Oh J.-S.a · Rhee J.-H.a, b · Cho B.-H.c · Lee H.-C.a, b
aDepartment of Microbiology, Chonnam National University Medical School, Brain Korea 21 Project, Center for Biomedical Human Resources at Chonnam National University, bClinical Vaccine R&D Center and Genome Research Center for Enteropathogenic Bacteria, and cDepartment of Nursing, College of Nursing, Chonnam National University, dDepartment of Allergy, Chonnam National University Medical School, Gwangju, and eLaboratory of Immunology, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea Int Arch Allergy Immunol 2009;150:32–42 (DOI:10.1159/000210378)


Background: Asthma is a major health problem worldwide, and the morbidity and mortality caused by asthma are on the rise. Corticosteroid therapies for asthma treatment frequently induce many side effects. Therefore, the development of new medicines that have both high efficacy and fewer side effects has been a scientific challenge. Here we tested the effect of ginsan, a polysaccharide derived from Panax ginseng, against allergic reaction in an ovalbumin (OVA)-induced murine asthmatic model in comparison with dexamethasone, and investigated its underlying mechanism. Methods: To induce murine asthma, mice were sensitized and challenged with OVA. Ginsan or dexamethasone was administered by injection 3 times a week. Airway hyperresponsiveness, airway inflammation and lung pathology were assessed in order to evaluate the effect of ginsan against asthma. Results: Ginsan treatment reduced airway hyperresponsiveness, remodeling and eosinophilia. These effects of ginsan were equivalent to those of dexamethasone. Ginsan treatment decreased the IL-5 level in the supernatant of cultured splenocytes, while IFN-γ and serum IgE were not altered. To elucidate the mechanism of ginsan, expression of inflammation-related genes were screened. Interestingly, ginsan treatment upregulated cyclooxygenase (COX)-1 and COX-2 mRNA, and expression of their proteins in the lung were also increased. PGE2 in the bronchoalveolar lavage fluid was also increased by the ginsan treatment. Lastly, ginsan inhibited the allergic reaction aggravated by COX inhibitor (indomethacin). Conclusion: Ginsan has anti-asthmatic effects, which seem to be partially mediated by enhancing the synthesis of COX gene products.


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