Biol. Pharm. Bull. 27(6) 825—830 (2004)

drug for the prevention of bronchial asthma and allergic rhinitis attacks. DSCG inhibits the release of chemical mediators, including histamine and tumor necrosis factor, from mast cells. While DSCG is known to induce intracellular signaling events associated with physiological and pathological processes, the molecular mechanisms of DSCGinduced signaling have remained unclear. Recent evidence, however, also demonstrates that DSCG has an antiviral effect on upper respiratory tract infection. In in vivo studies, DSCG significantly reduced expression of ICAM-1, a receptor for rhinoviruses. This drug also inhibits the cytopathic effects induced by certain viruses in vitro. The mechanisms of DSCG viral inhibition have not been elucidated. Inhalation or intranasal administration of DSCG was effective for the treatment of acute upper respiratory tract infection in children. Additional studies, however, have suggested that DSCG is not effective against viral infection either in vitro or in vivo. A recent randomized trial examining the effect of DSCG on acute upper respiratory tract viral infection showed that intranasal administration of DSCG was not effective against viral infection. Thus, the effect of DSCG on acute upper respiratory tract viral infections remains controversial. The chemical structure of DSCG is similar to flavonoids and related derivatives of cromolyn compounds (Fig. 1). Several flavonoids demonstrate anti-influenza effects and inhibition of influenza virus neuraminadases. In this study, we investigated the effects of DSCG on viral infection, particularly on human influenza virus infection in vivo. We determined that DSCG exerts anti-influenza virus effects both in vitro and in vivo. These findings indicate that DSCG may be an effective agent for prevention of human including children from influenza virus infection.