Abstract
Fulminant hepatic failure (FHF), associated with high mortality, is characterized by extensive death of hepatocytes and hepatic dysfunction. There is no effective treatment for FHF. Several studies have indicated that flavonoids can protect the liver from different factor-induced injury. Previously, we found that the extracts of Elaeagnus mollis leaves had favorable protective effects on acute liver injury. However, the role and mechanisms behind that was elusive. This study examined the hepatoprotective mechanisms of kaempferol-3-O-α-l-arabinopyranosyl-7-O-α-l-rhamnopyra-noside (KAR), a major flavonol glycoside of E. mollis, against d-galactosamine (GalN) and lipopolysaccharide (LPS)-induced hepatic failure. KAR reduces the mouse mortality, protects the normal liver structure, inhibits the serum aspartate aminotransferase (AST) and alamine aminotransferase (ALT) activity and decreases the production of malondialdehyde (MDA) and reactive oxygen species (ROS) and inflammatory cytokines, TNF-α, IL-6, and IL-1β. Furthermore, KAR inhibits the apoptosis of hepatocytes and reduces the expression of TLR4 and NF-κB signaling pathway-related proteins induced by GalN/LPS treatment. These findings suggest that the anti-oxidative, anti-inflammatory, and anti-apoptotic effects of KAR on GalN/LPS-induced acute liver injury were performed through down-regulating the activity of the TLR4 and NF-κB signaling pathways.
Highlights
Fulminant hepatic failure (FHF), known as acute liver failure (ALF), is a serious liver injury caused by a variety of factors, such as viruses, drugs, poisons, alcohol, pregnancy, autoimmune liver diseases, hereditary metabolic disorder, cholestasis, etc., which is associated with high mortality and accompanied with hepatic encephalopathy, severe coagulation dysfunction, jaundice, or hydroperitoneum
Results showed that serum AST and ALT levels increased significantly after microstructure and serum AST
Results showed that the levels of MDA and reactive oxygen species (ROS) and the production of tumor necrosis factor (TNF)-α, IL-1β, and IL-6 in the serum and liver tissues were significantly increased after GalN/LPS treatment, and this could be attenuated by pretreatment with KAR
Summary
Fulminant hepatic failure (FHF), known as acute liver failure (ALF), is a serious liver injury caused by a variety of factors, such as viruses, drugs, poisons, alcohol, pregnancy, autoimmune liver diseases, hereditary metabolic disorder, cholestasis, etc., which is associated with high mortality and accompanied with hepatic encephalopathy, severe coagulation dysfunction, jaundice, or hydroperitoneum. The mechanism involved in pathogens or toxicants induced FHF includes two aspects. Pathogens or toxic substances directly damage the structure and organelles of liver cells and trigger series of cell signaling cascade, which lead to the disorders of cell structure and function, and induce cell apoptosis or necrosis. Great progress has been made in the pathogenesis and diagnosis of FHF, there is still no effective treatment. More and more researchers focus on looking for more effective medication of FHF [3,4,5,6,7]
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