Mediators of Inflammation

Mediators of Inflammation / 2001 / Article

Open Access

Volume 10 |Article ID 420940 |

Shinya Sakai, Hiroshi Ochiai, Naoki Mantani, Toshiaki Kogure, Naotoshi Shibahara, Katsutoshi Terasawa, "Administration of isoferulic acid improved the survival rate of lethal influenza virus pneumonia in mice", Mediators of Inflammation, vol. 10, Article ID 420940, 4 pages, 2001.

Administration of isoferulic acid improved the survival rate of lethal influenza virus pneumonia in mice


Background: Isoferulic acid (IFA) is a main active ingredient of the rhizoma of Cimicifuga heracleifolia, which is used frequently in Japanese traditional medicine as an anti-inflammatory drug. It has been revealed that IFA inhibits the production of macrophage inflammatory protein-2 (MIP-2), which is a murine counterpart of the chemokine family that may contribute to the pathogenesis of inflammatory diseases through the chemotactic activity for inflammatory and immune effector cells.Aim of the study: In this study, we investigated the therapeutic effect of IFA on the progression of lethal influenza virus pneumonia in mice by comparison with that of dexamethasone (DX), a potent inhibitor for various inflammatory cytokines including MIP-2.Methods: Mice were infected by intranasal inoculation of influenza virus under ether anesthesia. The IFA or DX was given by oral administration once daily for 4 days after infection. After infection, the survival rate and the change in body weight were daily monitored.Results: IFA administration markedly improved the survival rate and body weight loss of influenza virusinfected mice in a suitable dose range (0.5 mg/day). However, DX administration did not show a beneficial effect at any dose.Conclusion: These data suggested that IFA is a novel tool not only for the intervention therapy, but also for the studies on the pathogenesis of influenza virusinduced pneumonia.

Copyright © 2001 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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