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硫代乙酰胺诱导的肝衰竭大鼠脑的凝集素组织化学

Lectin histochemistry of the rat brain following thioacetamide-induced hepatic failure.

作者信息

Szumańska G, Albrecht J

机构信息

Department of Neuropathology, Polish Academy of Sciences, Warsaw, Poland.

出版信息

Mol Chem Neuropathol. 1997 Sep-Dec;32(1-3):163-77. doi: 10.1007/BF02815174.

DOI:10.1007/BF02815174
PMID:9437665
Abstract

Biotinyl derivatives of several lectins were used to study the localization of glycoconjugates in the cerebral microcapillaries and various brains of rats given at 24-h intervals two i.p. administrations of a hepatotoxin-thioacetamide (TAA) and examined 21 d posttreatment. At this time, the rats were asymptomatic with regard to hepatic encephalopathy but showed specific and selective changes in the blood-brain-barrier (BBB) transport of basic amino acid, but no BBB damage, and region-specific neuronal injury in the hippocampus and neocortex. The lectins tested recognized the following sugar residues: beta-D-galactosyl (Ricinus communis agglutinin [RCA-1]); N-acetyl-glucosaminyl and N-acetyl-neuraminic acid (wheat-germ agglutinin [WGA]); N-acetyl-D-galactosaminyl (Helix pomatia agglutinin [HPA]); beta-D-galactosyl and D-galactosyl neuraminic acid (peanut agglutinin [PNA]), and alpha-D-galactosyl and alpha-D-mannosyl (concanavalin A [Con A]). The treatment markedly decreased the binding to the cerebromicrovascular network of the hippocampus and neocortex of RCA-1 and WGA. The binding of these two lectins to their complementary monosaccharide residues appears to reflect subtle changes in BBB function, with a detection threshold below the conventional BBB permeability tests. The changes in the binding of the other two lectins: an increase of HPA binding and a decrease of Con A binding, confined to neocortical neurons and pyramidal cells of hippocampus injured by TAA treatment.

摘要

几种凝集素的生物素化衍生物被用于研究糖缀合物在脑微血管中的定位,以及给大鼠腹腔注射肝毒素硫代乙酰胺(TAA),每隔24小时注射一次,在治疗后21天检查的不同大鼠脑内糖缀合物的定位情况。此时,大鼠在肝性脑病方面无症状,但在碱性氨基酸的血脑屏障(BBB)转运中表现出特异性和选择性变化,不过没有血脑屏障损伤,且在海马体和新皮质中存在区域特异性神经元损伤。所测试的凝集素识别以下糖残基:β-D-半乳糖基(蓖麻凝集素[RCA-1]);N-乙酰葡糖胺基和N-乙酰神经氨酸(麦胚凝集素[WGA]);N-乙酰-D-半乳糖胺基(苹果蜗牛凝集素[HPA]);β-D-半乳糖基和D-半乳糖基神经氨酸(花生凝集素[PNA]),以及α-D-半乳糖基和α-D-甘露糖基(伴刀豆球蛋白A[Con A])。该治疗显著降低了RCA-1和WGA与海马体和新皮质的脑微血管网络的结合。这两种凝集素与其互补单糖残基的结合似乎反映了血脑屏障功能的细微变化,检测阈值低于传统的血脑屏障通透性测试。另外两种凝集素结合的变化:HPA结合增加和Con A结合减少,局限于受TAA治疗损伤的新皮质神经元和海马体锥体细胞。

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