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目的：阐明维生素Ａ缺乏（ＶＡＤ）引起大鼠红系祖细胞（ＥＰＣ）表面Ｎ连接型糖链结构改变从而导致ＥＰＣ增殖分化障碍的机理。方法：经３Ｈ－甘露糖掺入和结合外切糖苷酶的系列凝集素柱层析和凝胶过滤，研究ＶＡＤ大鼠骨髓基质细胞和脾细胞条件培养液（ＢＭＳＣＭ和ＳＣＭ）对正常大鼠ＥＰＣ表面Ｎ糖链结构的影响。结果：ＶＡＤ大鼠的ＢＭＳＣＭ和ＳＣＭ可致：３Ｈ－苷露糖掺入ＥＰＣ表面Ｎ糖肽的总量减少；高甘露糖型和杂合型糖链结构比例增大，复杂型的糖链结构比例下降；而在复杂型糖链中，二天线糖链的比例和不含分叉型Ｎ－乙酰基葡萄糖（Ｂ－Ｇｎ）和核心岩藻糖（Ｃ－Ｆｕｃ）的组分降低，含Ｂ－Ｇｎ或Ｃ－Ｆｕｃ或同时含Ｂ－Ｇｎ和Ｃ－Ｆｕｃ的组分增大。结论：ＶＡＤ可能影响造血生长因子（ＩＬ－３和ＧＭ－ＣＳＦ等）的表达／活性，因而导致ＥＰＣ表面糖链的异常以及ＥＰＣ增殖分化障碍。
OBJECTIVE: To elucidate the mechanism of vitamin A deficiency (VAD) -induced structural changes of N-linked glycans in rat erythroid progenitor cells (EPCs) resulting in EPC proliferation and differentiation disorders. Methods: A series of lectin column chromatography and gel filtration with incorporation of exo-glycosidase and 3H-mannose were used to investigate the effect of BMSCM and SCM on the proliferation of normal rat EPC Surface N sugar chain structure. Results: The BMSCM and SCM of VAD rats induced a decrease in the total amount of N-glycopeptides incorporated into 3H-glycoside-bound EPC surface. The ratio of high-mannose and heterozygous sugar chains increased. The complex sugar chain structure The proportion of the two-antennary sugar chains and the components without B-Gn and C-Fuc decreased in the complex type sugar chains, Gn or C-Fuc or both B-Gn and C-Fuc. Conclusion: VAD may affect the expression / activity of hematopoietic growth factors (IL-3, GM-CSF, etc.), resulting in abnormal sugar chain on the surface of EPC and obstacles of proliferation and differentiation of EPCs.