concanavalin-a and astilbin

The aim of this study was to evaluate the effect of astilbin on concanavalin A (Con A)-induced hepatitis, a T cell-dependent model of liver injury. Con A administration resulted in a severe liver injury in mice, with a strong increment in spleen cell adhesion and liver infiltration of T cells, as well as in tumour necrosis factor (TNF)-alpha production. Against this liver injury, astilbin significantly inhibited the elevation in transaminase activity, reduced the TNF-alpha production, and improved the histological changes, including inflammatory infiltration, hepatocyte necrosis and degeneration and Kupffer cell hyperplasia. In addition, astilbin inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver-injured mice to fibronectin, laminin and type IV collagen.Moreover, the adhesion of human Jurkat T cells to endothelial cell line ECV-304 was also inhibited by astilbin. These results suggest that the improvement of the T cell-mediated liver injury by astilbinmay be related to the reduction in TNF-alpha production and in T cell adhesion to extracellular matrices and endothelial cells.

Topics: Animals; Cell Adhesion; Chemical and Drug Induced Liver Injury; Collagen Type IV; Concanavalin A; Extracellular Matrix; Female; Fibronectins; Flavonols; Humans; Jurkat Cells; Laminin; Liver; Male; Mice; Mice, Inbred ICR; Plant Extracts; Smilax; T-Lymphocytes; Tumor Necrosis Factor-alpha

To examine the therapeutic effects of astilbin, a flavanoid isolated from Rhizoma Smilacis Glabrae, on arthritis and to compare it with cyclosporine A (CsA).. Type II collagen-induced arthritis in mice and its in vitro assays for proliferation, matrix metalloproteinase (MMP) and NO production were performed.. Astilbin dose-dependently inhibited the footpad swelling, arthritic incidence, and clinical scores without influencing the body weights, while CsA showed strong inhibition with a significant weight loss. Histological examination revealed marked inflammatory damage in arthritic mice including joint swelling, synovial hyperplasia, and cartilage destruction. Against these, an intact joint structure was maintained in astilbin-treated or CsA-treated mice. In isolated spleen cells from arthritic mice, increased potentials in proliferation, NO production, and MMP-2 and 9 activities were suppressed dose-dependently by the oral administration of astilbin. Additionally, astilbin showed neither any cytotoxicity to nor influence on Con A-induced proliferation of spleen cells from naive mice, while CsA showed a dose-dependent cytotoxicity and inhibition of the proliferation.. Astilbin may act as an efficient therapeutic agent for arthritis like CsA but with less toxicity. Its mechanism includes a selective suppression on lymphocyte functions via reducing MMP and NO production.

Topics: Animals; Antirheumatic Agents; Arthritis, Experimental; Concanavalin A; Cyclosporine; Drugs, Chinese Herbal; Flavonols; Hindlimb; Lymphocytes; Male; Matrix Metalloproteinases; Mice; Mice, Inbred Strains; Nitric Oxide; Spleen