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   <subfield code="a">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</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Remina Ikeda, Kyoko Ishii, Yoshiko Hoshikawa, Junya Azumi, Yuta Arakaki, Toshihiro Yasui, Shizuka Matsuura, Yoshiaki Matsumi, Yohei Kono, Yusuke Mizuta, Akihiro Kurimasa, Ichiro Hisatome, Scott Friedman, Hironaka Kawasaki, Goshi Shiota]</subfield>
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   <subfield code="a">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.</subfield>
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