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Objectives The extract of Tupistra chinensis ( TCE) is traditionally used for the treatment of inflammatory diseases in southwestern China for hundreds of years. The present study was designed to investigate the effects of the TCE against experimental hepatitis and to illustrate its potential mechanisms. Methods Effects of TCE were investigated on Con A-induced hepatitis. Profiles of multiple cytokines were measured with biometric immuno-sandwich ELISA. Proliferation, activation and apoptosis of T lymphocytes were evaluated using Western blot, MTT analysis and flow cytometry. Key findings TCE significantly inhibited levels of serum transaminases and lactic dehydrogenase in mice with Con A-induced hepatitis, accompanied with marked alleviation of the liver microscopic appearances. Moreover, it decreased levels of inflammatory cytokines in a concentration-dependent manner both in vivo and in vitro. It also suppressed mitogen-activated protein kinases and NF-κ B-signalling in liver. These effects of TCE are attributed to its inhibition on activated T cells but not to hepatocytes protection. Flow cytometry and immunoblot assay data showed its effects on STAT1/ NF-κ B-signalling blockage and apoptosis induction in activated T cells. Conclusion Our findings illustrate the significant potential of TCE as a novel approach for treatment of T cell-mediated inflammatory diseases. [ABSTRACT FROM AUTHOR]

Objectives. Increasing evidence indicates that ezrin/radixin/moesin (ERM) proteins may play a critical role in cell proliferation. This study examined the role of ERM proteins in proliferation of fibroblast-like synoviocytes (FLS) from patients with RA.Methods. Synovial tissues (STs) were obtained from 18 RA and 6 OA patients. The expression of ERM and its phosphorylated proteins in cultured FLS and ST was assessed by western blots or IF staining. Small interference RNA (siRNA)-mediated ERM knockdown was used to inhibit phosphorylation of ERM. Proliferation of FLS was measured by bromodeoxyuridine (BrdU) incorporation into cell DNA and by PCNA immunoblotting.Results. Our study showed that increased phosphorylation of ERM proteins was found in ST and FLS from patients with RA as compared with OA patients and non-arthritis controls. Treatment with TNF-α, IL-1β or PDGF-induced phosphorylation of ERM proteins in dose- and time-dependent manner by RA FLS, but did not affect the expression of total ERM protein. Rho kinase and p38MAPK signal pathways were involved in TNF-α-induced ERM phosphorylation. We further showed that inhibition of ERM phosphorylation by siRNA-mediated ERM knockdown suppressed TNF-α- or IL-1β-induced BrdU incorporation and PCNA expression in RA FLS.Conclusions. This study provides the novel evidence that increased phosphorylation of ERM proteins may contribute to proliferation of RA FLS, suggesting that specific inhibition of ERM phosphorylation may be a new therapeutic approach for RA. [ABSTRACT FROM PUBLISHER]