HS-173, a Novel PI3K Inhibitor, Attenuates the Activation of Hepatic Stellate Cells in Liver Fibrosis

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Hepatic stellate cells (HSCs) are the primary source of matrix components in liver disease such as fibrosis. Phosphatidylinositol 3-kinase (PI3K) signaling in HSCs has been shown to induce fibrogenesis. In this study, we evaluated the anti-fibrotic activity of a novel imidazopyridine analogue (HS-173) in human HSCs as well as mouse liver fibrosis. HS-173 strongly suppressed the growth and proliferation of HSCs and induced the arrest at the G2/M phase and apoptosis in HSCs. Furthermore, it reduced the expression of extracellular matrix components such as collagen type I, which was confirmed by an in vivo study. We also observed that HS-173 blocked the PI3K/Akt signaling pathway in vitro and in vivo. Taken together, HS-173 suppressed fibrotic responses such as cell proliferation and collagen synthesis by blocking PI3K/Akt signaling. Therefore, we suggest that this compound may be an effective therapeutic agent for ameliorating liver fibrosis through the inhibition of PI3K signaling.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2013-12
Language
English
Article Type
Article
Keywords

I COLLAGEN EXPRESSION; GROWTH-FACTOR-I; PHOSPHATIDYLINOSITOL 3-KINASE; AKT; FIBROGENESIS; APOPTOSIS; RECEPTOR; PATHWAY; KINASE; PHOSPHORYLATION

Citation

SCIENTIFIC REPORTS, v.3

ISSN
2045-2322
DOI
10.1038/srep03470
URI
http://hdl.handle.net/10203/189678
Appears in Collection
CH-Journal Papers(저널논문)
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