Reactive oxygen species and NADPH oxidase 4 induced by transforming growth factor β1 are the therapeutic targets of polyenylphosphatidylcholine in the suppression of human hepatic stellate cell activation

Objective and design To clarify the molecular mechanism of polyenylphosphatidylcholine (PPC), we examined the involvement of reactive oxygen species (ROS) and NADPH oxidase 4 (Nox4) in human hepatic stellate cells (HSCs). Material Using human LX-2 HSC cells, we examined the effects of PPC on express...

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Published inInflammation research Vol. 60; no. 6; pp. 597 - 604
Main Authors Ikeda, Remina, Ishii, Kyoko, Hoshikawa, Yoshiko, Azumi, Junya, Arakaki, Yuta, Yasui, Toshihiro, Matsuura, Shizuka, Matsumi, Yoshiaki, Kono, Yohei, Mizuta, Yusuke, Kurimasa, Akihiro, Hisatome, Ichiro, Friedman, Scott L., Kawasaki, Hironaka, Shiota, Goshi
Format Journal Article
LanguageEnglish
Published Basel SP Birkhäuser Verlag Basel 01.06.2011
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Summary:Objective and design To clarify the molecular mechanism of polyenylphosphatidylcholine (PPC), we examined the involvement of reactive oxygen species (ROS) and NADPH oxidase 4 (Nox4) in human hepatic stellate cells (HSCs). Material Using human LX-2 HSC cells, we examined the effects of PPC on expression of α-smooth muscle actin (α-SMA) and collagen 1, generation of ROS, Nox4 expression, p38 activation and cell proliferation, induced by transforming growth factor β1 (TGFβ1). Results PPC suppressed ROS which are induced by TGFβ1, phosphorylation of p38MAPK, and expression levels of α-SMA and collagen 1 in a dose-dependent manner. Higher concentrations of PPC also suppressed Nox4 levels. Conclusion These results suggest that ROS and Nox4 induced by TGFβ1 are the therapeutic targets of PPC in the suppression of human hepatic stellate cell activation.
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ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-011-0309-6