脑急性缺血期鞘糖脂糖基转移酶的变化

阻断ＳＤ大鼠大脑中部动脉（ｍｉｄｄｌｅｃｅｒｅｂｒａｌａｒｔｅｒｙ，ＭＣＡ）近端主干，制备了局灶性脑缺血模型，并观察到脑急性缺血期脑组织内鞘糖脂含量有十分显著的变化。为了解鞘糖脂变化的机制，作者利用同位素掺入法及简易的ＳｅｐｈａｄｅｘＧ－５０（Ｆｉｎｅ）柱层析法分离同位素标记的产物与底物的方法，研究了脑急性缺血后１／２、６、７２ｈ时缺血侧及非缺血侧大脑半球几种鞘糖脂糖基转移酶的变化。结果显示，阻断大脑中部动脉（ＭＣＡＯ）后７２ｈ内，缺血侧半球ＣＭＰ－ＮｅｕＡｃ：ＣＭＨ唾液酸转移酶（ＳＴ３）活性进行性升高，而其他三种唾液酸转移酶（ＳＴ１、ＳＴ２、ＳＴ４）及ＵＤＰ－ＧａｌＮＡｃ：ＧＭ３Ｎ－乙酰氨基半乳糖转移酶均呈不同程度的下降；另两种糖基转移酶ＵＤＰ－Ｇａｌ：ＣＭＨ半乳糖转移酶和ＵＤＰ－Ｇａｌ：ＧＭ３半乳糖转移酶则先行升高，再分别于ＭＣＡＯ后１／２和６ｈ后开始回降。实验结果提示，脑急性缺血期脑组织鞘糖脂的变化与鞘糖脂糖基转移酶活性的改变有密切关系。

CHANGES OF GLYCOSYLTRANSFERASES DURING ACUTE CEREBRAL FOCAL ISCHEMIA

Contents of glycosphingoliplds in rat brain change greatly during acute cerebral focal ischemia established by middle cerebral artery ocolusion(MCAO).In order to understand the mechanism underlying the glycosphingolipids aclteration,several glycosyltransferases, which are responsible for glycosphingolipids synthesis,were assayed, in tissues of ischemic and non-isc hemichemispheres, at 0.5, 6, and 72 hours following MCAO, by taking glycosphingolipids as acceptors of isotope labelled sugar nucleotides and utilizing Sephadex G-50(fine) column chromatograhpy to seperate substrates and reaction products. The reslut showed that, in ischemic hemispheres, enzyme activity of CMP-NeuAc: CMH sialyltransferase(ST3) was increased progressively in 72hr after MACO, while that of CMP-NeuAc:CDH sialyltransferase(ST1), CMP-NeuAc: CM3 sialyltransferase (ST2), CMP-NeuAc:GM1 sialyltransferase(ST4) , and UDP-GalNAc:GM3 N-Acetyl-galactosaminyltransferase lowered to varied extents, and transiant increament at beginning and followed decline was found in activity levels of both UDP-Gal: CMH galactosyltransferase and UDP-Gal: GM2 galactosyltransferase.Above enzymatic alteration parallels the glycosphingolipids changes accompaning acute cerebral focal ischemia.