摘要:目的探讨位于非胱硫醚β-合成酶(cystathionine β-synthase,CBS)区域的PRKAG2基因G100S突变对小鼠心肌细胞单磷酸腺苷活化蛋白激酶(AMPK)活性的影响。方法建立人源PRKAG2(G100S)转基因小鼠模型,分别随机选取N4代4周龄、12周龄的转基因小鼠和同窝野生型小鼠各6只,用磷酸化检测试剂盒检测小鼠心肌细胞中AMPK活性,比较转基因小鼠与同窝野生型小鼠AMPK活性的差异,并观察随着周龄的增长转基因小鼠AMPK活性的变化。结果4周龄和12周龄的转基因小鼠心肌细胞中AMPK活性均低于同窝野生型小鼠(0.042±0.013vs0.063±0.013,0.032±0.008vs0.062±0.018),差异均有统计学意义(P=0.019,P=0.004)。12周龄和4周龄的转基因小鼠心肌细胞中AMPK活性差异无统计学意义(P=0.135)。结论PRKAG2基因G100S突变可导致转基因小鼠心肌细胞AMPK活性下降,而且AMPK活性并不随着转基因小鼠周龄的增长而变化。
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