Abstract
BackgroundNowadays, treatments for cholestasis remain largely nonspecific and often ineffective. Recent studies showed that inflammatory injuries and oxidative stress occur in the liver with cholestasis. In this study, we would use corilagin to treat the animal model of acute cholestasis in order to define the activity to interfere with inflammation-related and oxidative stress pathway in cholestatic pathogenesis.MethodsRats were administrated with alpha-naphthylisothiocyanate to establish model of cholestasis and divided into corilagin, ursodeoxycholic acid, dexamethasone, model and normal groups with treatment of related agent. At 24h, 48h and 72h time points after administration, living condition, serum markers of liver damage, pathological changes of hepatic tissue, nuclear factor (NF)-kappaB, myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were examined and observed.ResultsCompared to model group, corilagin had remarkable effect on living condition, pathological manifestation of liver tissue, total bilirubin, direct bilirubin, (P<0.01), but no effect on alanine aminotransferase (ALT) and aspartate aminotransferase (AST). With corilagin intervention, levels of MPO, MDA and translocation of NF-κB were notably decreased, and levels of SOD and NO were markedly increased (P<0.05 or P<0.01).ConclusionsIt is shown that corilagin is a potential component to relieve cholestasis through inflammation-related and oxidation-related pathway.
Highlights
Nowadays, treatments for cholestasis remain largely nonspecific and often ineffective
Cholestasis is a reduction in bile flow that leads to the intrahepatic accumulation of bile acids and other toxic compounds with progression of liver pathology, including hepatocellular injury and fibrosis [1]
In order to obtain an effect in acute cholestasis in non-surgery condition, such as acute hepatitis, hepatic failure or drug-induced hepatic injury, UDCA should be combined with corticosteroids [9], which indicated that UDCA was a limited choice in those diseases
Summary
Treatments for cholestasis remain largely nonspecific and often ineffective. Inflammatory stimulators induce signaling pathways within hepatocytes either directly, or through activation of proinflammatory cytokines, which result in suppressed expression and function of key hepatobiliary transporters and repressed expression and activity of a large number of nuclear transcriptional regulators, subsequently leading to rapid and profound reductions in bile flow [3]. This procedure enrolls neutrophils to accumulate in the liver that evoke reactive oxygen species (ROS) to produce oxidative stress and liver injury [4]. The side effects of glucocorticoids limit use in many infection or bleeding-associated diseases
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