Reactive oxygen species and NADPH oxidase 4 induced by transforming growth factor beta 1 are the therapeutic targets of polyenylphosphatidylcholine in the suppression of human hepatic stellate cell activation

• Published in: Inflammation research 2011-06, Vol.60 (6), p.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: Article
• Language: English
• ISSN: 1023-3830; 1420-908X
• DOI: 10.1007/s00011-011-0309-6

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 alpha -smooth muscle actin ( alpha -SMA) and collagen 1, generation of ROS, Nox4 expression, p38 activation and cell proliferation, induced by transforming growth factor beta 1 (TGF beta 1). Results: PPC suppressed ROS which are induced by TGF beta 1, phosphorylation of p38MAPK, and expression levels of alpha -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 TGF beta 1 are the therapeutic targets of PPC in the suppression of human hepatic stellate cell activation.