The aberrant sugar chains of amylase and different TCM syndrome patterns in primary hepatic cancer as well as the related mechanism / 肿瘤

ABSTRACT

Objective: To investigate the changes of sugar chain structures of serum amylase and difference in TCM syndrome patterns in primary hepatic cancer (PHC) patients and their relation with free radicals. Methods: Agglutinin precipitation assay was used to detect the binding ratios of serum amylase with various kinds of agglutinin in PHC, hepatocirrhosis, and hepatitis patients. The serum amylase activity and malindialdehyde (MDA) level were determined simultaneously. The association of the binding ratios of amylase with free radicals was analyzed. The difference mentioned above in PHC patients with different TCM syndromes was analyzed. Results: The binding ratios of serum amylase to ConA, PSA, PNA, and LCA were significantly higher in PHC and hepatocirrhosis patients than hepatitis patients and normal controls. The binding ratios of serum amylase to PSA and LCA were significantly higher in PHC patients with spleen deficiency and liver stagnation than those with liver and kidney Yin deficiency. PHC patients with spleen deficiency and liver stagnation had higher ConA-binding ratio compared with those with QI and blood stasis. A positive correlation was found between PSA-, LCA-, and PNA-binding ratios of serum amylase and MDA. Conclusion: For PHC and hepatocirrhosis patients, core-fucosylated high-mannose-type and hybrid-type sugar chains of serum amylase increased. The reduced terminal sialic acid and fucose on the sugar chain caused the exposure of the terminal galactose residues. In addition, the exposure of the terminal GlcNAc residues was induced by decreased terminal galactose on the sugar chain of serum amylase from HPC patients. These changes of serum amylase were also observed in hepatocirrhosis patients. It may be related with the damage of sugar chains induced by free radicals. In spleen deficiency and liver stagnation group, core-fucosylated high-mannose-type and hybrid-type sugar chains of serum amylase increased, and the terminal galactose on the sugar chain decreased, resulting in the exposure of the terminal GlcNAc residues. The changes were not observed in QI and blood stasis or liver and kidney Yin deficiency patients. It indicated that spleen deficiency and liver stagnation played an important role in generation of aberrant sugar chains of serum amylase for PHC patients.