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肝癌患者淀粉酶糖链异常、证型差异及相关机制 被引量:5

The aberrant sugar chains of amylase and different TCM syndrome patterns in primary hepatic cancer as well as the related mechanism
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摘要 目的:研究肝癌患者的血清淀粉酶糖链变化、中医证型差异及与自由基的相关性。方法:凝集素亲和沉淀法检测肝癌患者、肝硬化患者、肝炎患者血清淀粉酶的多种凝集素结合率;同时检测血清丙二醛(m alind ialdehyde,MDA)、血清淀粉酶活性,分析淀粉酶的各凝集素结合率与自由基的相关性,分析以上指标在不同证型肝癌患者间的差异。结果:肝癌患者血清淀粉酶的ConA、PSA、PNA、LCA结合率明显高于肝炎组及正常组;肝硬化组淀粉酶的ConA、PSA、PNA、LCA的结合率亦明显高于肝炎组及正常组,肝癌肝郁脾虚患者血清淀粉酶的PSA、LCA的结合率明显高于肝癌肝肾阴虚患者,肝癌肝郁脾虚患者血清淀粉酶的ConA结合率明显高于肝癌气滞血瘀患者;血清淀粉酶的PSA、PNA、LCA结合率与MDA水平呈显著正相关。结论:肝癌患者血清淀粉酶分子中核心岩藻糖基化的高甘露糖型、杂合型糖链增多,其糖链末端唾液酸基、岩藻糖基减少,致D-半乳糖的暴露增多,此外,肝癌患者血清淀粉酶糖链末端D-半乳糖基亦减少,致N-乙酰氨基葡萄糖基暴露增多,肝硬化患者血清淀粉酶糖链亦有以上变化,这可能与自由基损害糖链有关。肝癌肝郁脾虚患者血清淀粉酶分子中核心岩藻糖基化的高甘露糖型、杂合型糖链增多,其糖链末端的D-半乳糖基减少,致N-乙酰氨基葡萄糖基暴露增多;而肝癌气滞血瘀和肝癌肝肾阴虚患者血清淀粉酶糖链无此变化,表明肝郁脾虚在肝癌患者血清淀粉酶异常糖链的形成方面可能起重要作用。 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, corefucosylated 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.
出处 《肿瘤》 CAS CSCD 北大核心 2008年第4期322-325,共4页 Tumor
基金 国家自然科学基金重大研究计划重点项目-子项目(编号:90209004)
关键词 肝肿瘤 辨证分型(中医) 淀粉酶类 自由基 Liver neoplasms Syndrome differ classification(TC) Amylases Free radicals
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