Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158
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Immunomodulatory Effects of Gyokuheifusan on INF-γ/IL-4 (Th1/Th2) Balance in Ovalbumin (OVA)-Induced Asthma Model Mice
Su-ping FangTakeshi TanakaFumitosi TagoTakuya OkamotoShuji Kojima
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2005 Volume 28 Issue 5 Pages 829-833

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Abstract

Asthma, a common, chronic lung disease in industrialized countries, is characterized by the production of large quantities of IgE antibody by B cells and a decrease of the IFN-γ/IL-4 (Th1/Th2) ratio. Gyokuheifusan (GHS) is a classical formulation of traditional Chinese medicine (TCM) that is usually prescribed to prevent or treat respiratory tract diseases, such as respiratory infection and bronchial asthma. In order to evaluate the possible effectiveness of GHS on bronchial asthma, its immunomodulatory activity was examined in ovalbumin (OVA)-induced asthma model mice. All mice, except those in the normal group, were sensitized by intraperitoneal (IP) administration of OVA emulsified with Al(OH)3, and a second immunization was given 6 d later. After a further 13, 17 and 21d, mice were challenged with inhalation of aerosolized OVA solution, except for the normal group, which received mock sensitization using saline-Al(OH)3 emulsion and were challenged with an aerosol of saline without OVA. Allergen-specific IgE and total IgE in plasma were both significantly increased in the disease-control group. These increases were markedly blocked by GHS treatment. IFN-γ released by splenocytes was significantly increased after co-culture with OVA for 24 h, 48 h, and 72 h. GHS treatment further elevated the IFN-γ content compared with the disease-control group. The production of IL-4 was significantly increased when splenocytes were simulated with OVA for 72 h, but this increase was blocked by GHS treatment, so that GHS returned the decreased IFN-γ/IL-4 (Th1/Th2) ratio of the disease-control group to the normal range. These results indicate that GHS may inhibit the development and severity of asthma.

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© 2005 The Pharmaceutical Society of Japan
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