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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。
To study the changes of protein phosphorylation dephosphorylation in the brain of ischemic mice after the mice were subjected to the decapitation cerebral ischemia. Phosphorylation of phosphorylated dephosphorylation in the brain of 1 min ischemia, 5 min, 15 min and 30 min in control mice showed that the phosphorylation of some phosphoproteins, such as 145 kD, 84 kD, 59 kD and 50 kD, weakened as the ischemic time prolonged, and some Phosphoproteins such as 119kD, 105kD, 78kD and 55kD phosphorylation increase with prolonged ischemia. Phosphorylation of PKA, PKC, Ca ~ (2 +) / CaMPK substrates in the cytoplasm and membrane of cerebral ischemia-reperfusion mice with significant changes in phosphorylation was studied. The results showed that calcium-related PKC , Phosphorylation of Ca ~ (2 +) / CaMPK substrate was significantly reduced in the ischemic rat brain. At the same time, the only calcineurin (CaN) substrate dependent on Ca ~ (2 +) / CaM in brain was studied. The phosphorylation of some CaN substrates in the brain of ischemic mice was decreased.