Open AccessT upistra chinensis extract attenuates murine fulminant hepatitis with multiple targets against activated T lymphocytes
Author(s) -
Wu Xuefeng,
Fan Jinjin,
Ouyang Zijun,
Ning Rui,
Guo Wenjie,
Shen Yan,
Wu Xudong,
Sun Yang,
Xu Qiang
Publication year - 2014
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1111/jphp.12176
Subject(s) - flow cytometry , apoptosis , western blot , fulminant hepatitis , pharmacology , in vivo , immunology , microbiology and biotechnology , biology , chemistry , hepatitis , biochemistry , gene
Objectives The extract of T upistra chinensis ( TCE ) is traditionally used for the treatment of inflammatory diseases in southwestern C hina 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 C on A ‐induced hepatitis. Profiles of multiple cytokines were measured with biometric immuno‐sandwich ELISA . Proliferation, activation and apoptosis of T lymphocytes were evaluated using W estern blot, MTT analysis and flow cytometry. Key findings TCE significantly inhibited levels of serum transaminases and lactic dehydrogenase in mice with C on 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.