缺血与正常小鼠脑内蛋白磷酸化脱磷酸化的比较研究

以小鼠断头脑缺血为模型，研究缺血小鼠脑内蛋白磷酸化脱磷酸化的改变。对缺血１ｍｉｎ、５ｍｉｎ、１５ｍｉｎ和３０ｍｉｎ及对照小鼠脑内蛋白磷酸化脱磷酸化的研究表明，有些磷蛋白如１４５ｋＤ、８４ｋＤ、５９ｋＤ和５０ｋＤ的磷酸化随缺血时间延长而减弱，还有些磷蛋白如１１９ｋＤ、１０５ｋＤ、７８ｋＤ和５５ｋＤ的磷酸化随缺血时间延长而增加。对磷酸化程度变化显著的缺血１５ｍｉｎ小鼠脑内胞浆及膜上ＰＫＡ、ＰＫＣ、Ｃａ~（２＋）／ＣａＭＰＫ底物的磷酸化进行了研究，发现胞浆组分中与钙相关的ＰＫＣ、Ｃａ~（２＋）／ＣａＭＰＫ底物磷酸化在缺血鼠脑中明显减弱。同时研究了脑内唯一依赖于Ｃａ~（２＋）／ＣａＭ的钙调神经磷酸酶（Ｃａｌｃｉｎｅｕｒｉｎ，ＣａＮ）底物的变化，发现缺血小鼠脑内ＣａＮ的某些底物磷酸化降低。

Protein Phosphorylation and Dephosphorylation in Ischmia and Normal Mice Brains

Phosphorylation and dephosphorylation of proteins in normal mice brain and mice brains subjected to 1min, 5min, 15min and 30min ischemia were detected by SDS-PAGE or 2D-PAGE and autoradiography. Decrease of phosphorylation of 145kD, 84kD, 59kD, 50kD phosphoproteins and increase of phosphorylation of 119kD, 105kD, 78kD, 55kD phosphoproteins in ischemia mice brains were detected. Decrease of phosphorylation of substrates of PKC, Ca￣(2+) /CaM PK in cytosolic fraction of ischemia mice brains and decrease of phosphorylation of some endogenous substrates of CaN in ischemia mice brains were also detected.