Digestive diseases and sciences · 2012
Hepatic stimulator substance alleviates toxin-induced and immune-mediated liver injury and fibrosis in rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Yi Xuerui, Song Ming, Yuan Youcheng, Zhang Xinrui, Chen Wenyin, Li Jin, Tong Minghua, Liu Guangze, You Song, Kong Xiangping
Аннотация
BACKGROUND: Liver fibrosis is a common scarring response to chronic liver injury. It is a precursor to cirrhosis and liver carcinoma. Hepatic stimulator substance (HSS), a known liver-specific but species-nonspecific growth factor, has been shown to protect hepatocytes from various toxins.
METHODS: We have investigated the effects of HSS therapy on carbon tetrachloride (CCl(4))-induced and porcine-serum-mediated hepatic injury and fibrosis. We hypothesize that HSS might attenuate liver injury and fibrosis by suppressing oxidative stress, down-regulating profibrogenic factors, and blocking HSCs activation.
RESULTS: This report demonstrated that HSS therapy diminished α-smooth muscle actin expression, decreased intrahepatic reactive oxygen species (ROS) level, and down-regulated transforming growth factor (TGF)-β1, platelet-derived growth factor (PDGF)-BB, and tissue inhibitor of metalloproteinase (TIMP)-1 expression. In addition, HSS treatment significantly protected the liver from injury by improving liver function tests and histological architecture of the liver.
CONCLUSIONS: These results provided novel insights into the mechanisms of HSS in the protection of the liver. Our results suggested that HSS might be a therapeutic antifibrotic agent for the treatment of liver fibrosis.
METHODS: We have investigated the effects of HSS therapy on carbon tetrachloride (CCl(4))-induced and porcine-serum-mediated hepatic injury and fibrosis. We hypothesize that HSS might attenuate liver injury and fibrosis by suppressing oxidative stress, down-regulating profibrogenic factors, and blocking HSCs activation.
RESULTS: This report demonstrated that HSS therapy diminished α-smooth muscle actin expression, decreased intrahepatic reactive oxygen species (ROS) level, and down-regulated transforming growth factor (TGF)-β1, platelet-derived growth factor (PDGF)-BB, and tissue inhibitor of metalloproteinase (TIMP)-1 expression. In addition, HSS treatment significantly protected the liver from injury by improving liver function tests and histological architecture of the liver.
CONCLUSIONS: These results provided novel insights into the mechanisms of HSS in the protection of the liver. Our results suggested that HSS might be a therapeutic antifibrotic agent for the treatment of liver fibrosis.
Предметные рубрики MeSH
AnimalsBecaplerminCarbon Tetrachloride PoisoningChemical and Drug Induced Liver InjuryHepatic Stellate CellsIntercellular Signaling Peptides and ProteinsLiverLiver CirrhosisLiver Function TestsMaleMitogensOxidative StressPeptidesProto-Oncogene Proteins c-sisRatsRats, Sprague-DawleyReactive Oxygen SpeciesSwineTissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1