concanavalin-a and baicalin

Baicalin (BA), a flavonoid compound isolated from Scutellaria baicalensis, has been shown to possess a number of pharmacological effects including antiviral, anti-inflammatory, antioxidant and immune regulation. Here, we examined its effects on human T and B cells proliferation by MTT assay and found that BA stimulated T and B cells proliferation, independently and cooperatively with Con-A (T cells) or LPS (B cells). Then, we analyzed the effects of BA treatment on the mRNA expression of Toll-like receptors (TLRs), IL-2, IFN-γ and IL-12 in T and B cells by real-time RT-PCR and attempted to observe whether blocking TLR4 had influence on mRNA expression. We found that BA treatment significantly up-regulated TLR3, 7, 8 and 9 mRNA expressions in T and B cells, IL-2 and IFN-γ in T cells and IL-12 in B cells. The increased mRNA expressions were suppressed after blocking TLR4. We further analyzed the effects of BA treatment on TCR vβ and CD79 mRNA expression levels in T and B cells and explored whether blocking TCR (αβ) or BCR mIgM F(ab')(2) had an influence on mRNA expression. We found that BA treatment significantly improved TCR vβ and CD79 mRNA expression in T and B cells, respectively, and the improvements were all inhibited after blocking TCR (αβ) or BCR mIgM F(ab')(2). Our results suggested that BA participates in innate and adaptive immune regulation by up-regulating the mRNA expression of TLRs (3, 7, 8 and 9), IL-2, IFN-γ and IL-12 in T and B cells, which is mediated by TLR4, and by improving the mRNA expression of TCR vβ and CD79, which is mediated by TCR (αβ) and BCR mIgM, respectively. Therefore, TLR4, TCR (αβ) and BCR mIgM are all the immune receptors for BA on T and B cells.

Topics: Anti-Inflammatory Agents, Non-Steroidal; B-Lymphocytes; Cell Proliferation; Cells, Cultured; Concanavalin A; Cytokines; Flavonoids; Humans; Immunologic Factors; Lipopolysaccharides; Receptors, Antigen, B-Cell; Receptors, Antigen, T-Cell; T-Lymphocytes; Toll-Like Receptor 4; Toll-Like Receptors; Up-Regulation

Baicalin (BA) exhibits an anti-inflammatory effect in vivo and in vitro and is used to treat chronic hepatitis. However, the mechanism by which BA exerts the liver-protective effect remains largely unknown.. The present study reports that BA inhibits cytokine production and hepatocyte apoptosis to protect mice from liver injury induced by concanavalin A (Con A), a T-cell-dependent liver injury model.. Con A injection of mice induced severe immune responses and extensive hepatocellular apoptosis within 24 h. Pretreatment of 200 or 100 mg/kg BA markedly reduced serum aminotransferase activities, protected hepatoycte apoptosis and reduced the increase of plasma cytokine levels, including tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-6 (IL-6). Furthermore, BA pretreatment decreased tissue myeloperoxidase activity and lipid peroxidation, but increased the superoxide dismutase level. In vitro studies indicated that the beneficial effect of BA was associated with reduced cytokine production from lymphocytes and reduced TNF-alpha-induced hepatocyte apoptosis.. These results suggest that BA has therapeutic potential for T-cell-mediated liver injury.

Topics: Animals; Apoptosis; Chemical and Drug Induced Liver Injury; Concanavalin A; Cytokines; Flavonoids; Hepatocytes; Mice; Mice, Inbred Strains; Protective Agents; T-Lymphocytes; Treatment Outcome; Tumor Necrosis Factor-alpha