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
- First Online:
- Cite this article as:
- Ikeda, R., Ishii, K., Hoshikawa, Y. et al. Inflamm. Res. (2011) 60: 597. doi:10.1007/s00011-011-0309-6
- 397 Downloads
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).
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).
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.
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.
KeywordsPolyenylphosphatidylcholine NADPH oxidase 4 Hepatic stellate cells Oxidative stress
Hepatic stellate cell
Platelet-derived growth factor
Transforming growth factor β-1