白血病患儿尿淀粉酶糖链异常、证型差异及相关机理

The aberrant sugar chains of urinary amylase in children leukemia,of different TCM type

目的:研究白血病患儿尿淀粉酶糖链变化、证型差异及与自由基的相关性。方法:用凝集素亲和沉淀法检测25例脾胃虚弱型白血病患儿、11例肝郁气滞型白血病患儿、16例非白血病患儿尿液中淀粉酶多种凝集素结合率,凝集素包括PNA、ConA、LCA、PSA、L-PHA、WGA;同时检测尿液淀粉酶活性及自由基相关指标ONOO-、MDA。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白血病患儿间的差异。结果:白血病患儿的尿液淀粉酶活性均显著高于非白血病患儿,但不同证型间无显著性。白血病患儿尿液淀粉酶的PSA、PNA、ConA结合率显著高于非白血病患儿;其中仅脾胃虚弱型白血病患儿尿液淀粉酶的PNA、ConA、PSA、LCA结合率显著高于非白血病患儿;而肝郁气滞型白血病患儿尿液淀粉酶的各凝集素结合率均与非白血病患儿无显著差别。白血病患儿尿液ONOO-、MDA均显著低于非白血病患儿,但脾胃虚弱型白血病患儿尿液ONOO-、MDA均显著高于肝郁气滞型白血病患儿。相关分析发现,尿液淀粉酶的WGA、LCA、ConA、PSA结合率与MDA呈显著负相关。结论:白血病患儿尿液淀粉酶糖链发生显著变化,高甘露糖型及杂合型糖链显著增多,其糖链核心岩藻糖基升高,其糖链末端唾液酸基、岩藻糖基减少,D-半乳糖暴露增多,这一变化主要存在于脾胃虚弱型白血病患儿,而肝郁气滞型白血病患儿无此变化,这可能与自由基对淀粉酶糖链的损害有关,这说明脾胃虚弱在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 urinary amylase in children leukemia with different traditional Chinese medicine syndrome types, and its relation to free radical. Methods ： Lectins - binding ratios of urine amylase, urinary amylase activity, ONOO- , MDA were determined in children leukemia with spleen- deficiency and lever qi stagnation , children non - leukemia patients. Results： Urine amylase activity was elevated in children leukemia, as compared to children non - leukemia patients. In children leukemia, PNA.ConA.PSA - binding ratios of urine amylase were elevated, in children leukemia with spleen - deficiency, PNA, ConA, PSA, LCA - binding ratios of urine amylase were elevated, no significant variation in children leukemia with lever qi stagnation, as compared to children non - leukemia patients. Urine ONOO - , MDA of children leukemia were lower than that of children non - leukemia patients, however, urine ONOO - , MDA of children leukemia with spleen - deficiency were higher than that of children leukemia with lever qi stagnation. A negative correlation was found between WGA. LCA. ConA .PSA- binding ratios and MDA. Conclusion： In children leukemia, urine amylase core -fucosylated ,high - mannose-type, hybrid- type sugar chains increased , terminal sialic acid and fucose on the sugar chain decrease, this exist in only children leukemia with spleen - deficiency, not exist in children leukemia with lever qi stagnation, this may be caused by increasing free radical damage amylase sugar chains, maybe spleen - deficiency syndrome type play an important part in generating aberrant amylase sugar chains.