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Published in: Inflammation Research 6/2011

01-06-2011 | Original Research Paper

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

Authors: 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 L. Friedman, Hironaka Kawasaki, Goshi Shiota

Published in: Inflammation Research | Issue 6/2011

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Abstract

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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Metadata
Title
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
Authors
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 L. Friedman
Hironaka Kawasaki
Goshi Shiota
Publication date
01-06-2011
Publisher
SP Birkhäuser Verlag Basel
Published in
Inflammation Research / Issue 6/2011
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-011-0309-6

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