PMC:2783367 / 40876-41380 JSONTXT

{"project":"2_test","denotations":[{"id":"19736547-15307867-66178379","span":{"begin":99,"end":101},"obj":"15307867"},{"id":"19736547-15307867-66178379","span":{"begin":99,"end":101},"obj":"15307867"},{"id":"19736547-10335777-66178380","span":{"begin":237,"end":239},"obj":"10335777"},{"id":"19736547-10335777-66178380","span":{"begin":237,"end":239},"obj":"10335777"},{"id":"T43004","span":{"begin":99,"end":101},"obj":"15307867"},{"id":"T25847","span":{"begin":99,"end":101},"obj":"15307867"},{"id":"T10474","span":{"begin":237,"end":239},"obj":"10335777"},{"id":"T81354","span":{"begin":237,"end":239},"obj":"10335777"}],"text":"NASH patients are often associated with high levels of lipid peroxidation products, such as ox-LDL 44. It has been suggested that the elevated levels of lipid peroxidation might make an important contribution to the pathogenesis of NASH 45, leading to hepatic fibrosis. In the current report, we demonstrated that ox-LDL stimulated the activation of HSCs in vitro, which was attenuated by curcumin by suppressing gene expression of LOX-1 via the activation of PPARγ and the interruption of Wnt signaling."}