Evaluation of the mechanism of cordyceps polysaccharide action on rat acute liver failure.

Abstract

IntroductionThis study aimed to investigate the mechanism of action of cordyceps polysaccharide on rat acute liver failure (ALF).Material and methodsSixty rats were randomly divided into five groups: a normal group, a model group without cordyceps polysaccharide and groups with cordyceps polysaccharide in three different doses (5, 10 and 20 mg/ml). Serum alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) contents were measured for assessing liver function. Hematoxylin and eosin (HE) staining was used for observing liver pathology. Apoptosis was detected through the method of terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Protein expression levels of caspase-1, interleukin-18 (IL-18), IL-10, vascular endothelial growth factor (VEGF), and stromal cell-derived factor-1α (SDF-1α) in liver tissue were detected by Western blot. Proliferating cell nuclear antigen (PCNA) and signal regulatory protein-α1 (SIRPα1) contents were measured by PCR.ResultsThe rat ALF model was established with D-galactosamine induced by lipopolysaccharide (LPS). After modelling, tissue HE staining showed typical manifestation of acute liver injury that emerged in the rat ALF model. The liver failure group showed higher levels of serum ALT and AST, as well as hepatocyte apoptosis, than the groups treated with cordyceps polysaccharide. Cordyceps polysaccharide can effectively suppress the protein expression of caspase-1, IL-18, and IL-10, while simultaneously increasing the protein expression of VEGF and SDF-1α, as well as the mRNA expression of PCNA and SIRPα1.ConclusionsCordyceps polysaccharide can alleviate the immune response and inflammatory injury in ALF by regulating the balance of pro-inflammatory and anti-inflammatory factors and reducing the apoptosis.