Antiallergic herbal composition from Scutellaria baicalensis and Phyllostachys edulis.

We aimed to find antiallergic agents from natural sources using mast cells activated during allergic reaction. We screened over 2000 plants for blockade of histamine release and identified two of them, S. baicalenesis and P. edulis. Bioassay-guided fractionation led to two main constituent flavonoids, baicalin from S. baicalenesis roots and isoorientin from P. edulis leaves. Based on these two compounds, two standardized extracts (SSBE and SPEE) and a combined standardized herb composition (SHC) were developed. SSBE, SPEE, and SHC remarkably inhibited histamine and leukotriene release from mast cells activated by anti-OVA/OVA binding, and SHC showed a stronger inhibition than either extract alone. SHC also showed greater inhibition potency than either aspirin or cromolyn, which are known antiallergic agents. Our results suggest that SHC reduce degranulation during mast cell activation and could be a promising candidate for the treatment of immune/allergic diseases related to mast cells.

Regulation of lymphocyte clustering by CD30-mediated ICAM-1 up-regulation.

CD30 is expressed transiently on activated B and T lymphocytes and constitutively on several B- and T cell lymphomas. CD30 functions include participation in negative selection of thymocytes, costimulation of activated T cells, isotype switching of B cells, and regulation of the effector activity of cytotoxic lymphocytes. Although CD30 is not a marker for T helper 2 (TH2) cells, it may participate in the polarization of TH1 and TH2 cells. The pleiotropic functions of CD30 are initiated by interaction of CD30-expressing cells with other immune competent cells expressing CD30-L and providing the signals for modulation of effector cell activity. Here, we report that CD30 signals generated by anti-CD30 on activated, normal murine T cells strongly up-regulate the expression of intercellular adhesion molecule 1 (ICAM-1, CD54), and to a lesser extent, ICAM-2 (CD102). CD30 signals moreover delay the subsequent decline of ICAM expression. CD30 cross-linking did not alter the expression of CD11a/CD18 (LFA-1), the counter receptor for ICAM abundant on T cells. CD30-mediated ICAM-1 up-regulation is independent of cytokine secretion and appears to be transmitted directly through NF-kappaB activation. CD30-mediated up-regulation of ICAM-1 expression led to a significant increase in cluster formation of lymph node cells. Increased lymphocyte self-aggregation mediated by CD30 may set the stage for fraternal signaling to modulate lymphocyte function.