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2010年06月 アーカイブ

2010年06月25日

パラミロンに関する論文がパブリッシュされました

鳥取大学の杉山先生との共同研究の内容になります。ユーグレナにしか含有されない特有の物質であるパラミロンに関する可能性が、また一つ明らかになりました。

ユーグレナの利用の可能性に関して、今後も様々なことを追求していきたいと思います。

下記、URLからフルテキストの論文を読むことができます。
http://www.jstage.jst.go.jp/article/jvms/72/6/72_755/_article


Oral administration of paramylon, a beta-1,3-D-glucan isolated from Euglena gracilis Z inhibits development of atopic dermatitis-like skin lesions in NC/Nga mice.
Sugiyama A, Hata S, Suzuki K, Yoshida E, Nakano R, Mitra S, Arashida R, Asayama Y, Yabuta Y, Takeuchi T.

Course of Veterinary Laboratory Medicine, School of Veterinary Medicine, Faculty of Agriculture, Tottori University, Japan. sugiyama@muses.tottori-u.ac.jp

Abstract
Paramylon is a beta-1,3-D-glucan isolated from Euglena gracilis Z. This study was designed to evaluate the suppressive effects of the oral administration of paramylon on the development of atopic dermatitis (AD)-like skin lesions induced by repeated application of 2,4,6-trinitrochlorobenzene (TNCB) in sensitized NC/Nga mice. The effects of paramylon were assessed by measuring macroscopical and histopathological findings of skin, ear swelling, serum levels of total IgE, interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) and IL-18 and IL-12 contents in the skin lesions. Oral administration of paramylon inhibited the development of AD-like skin lesions as exemplified by a significant decrease in dermatitis scores for the back, ear swelling and hypertrophy of the skin, infiltration of inflammatory cells in the skin, and serum IgE levels. Oral administration of paramylon reduced serum levels of both IL-4 and IFN-gamma and IL-18 and IL-12 contents in the skin lesions. Oral administration of paramylon did not cause weight loss, as was observed with prednisolone. These results suggest that paramylon inhibits the development of AD-like skin lesions in NC/Nga mice by suppressing both the T-helper (Th) 1 and Th 2 cell responses. Our results indicate that paramylon treatment could provide an effective alternative therapy for the management of AD.