研究指出表沒食子兒茶素沒食子酸酯（EGCG）具有抗氧化的能力且能降低氧化壓力對心肌細胞所造成的傷害。雖然許多研究證實EGCG具有保護心臟的效果，但EGCG在細胞膜上的作用機制並不是十分地清楚。在本研究中，我們建立兩種實驗模式：一個是利用雙氧水使H9c2大鼠胚胎心肌細胞產生氧化壓力來模擬缺血再灌流的傷害；另一個則是將大鼠的左前降支冠狀動脈結紮建立心肌梗塞的動物模式。H9c2細胞受到雙氧水的傷害後會造成細胞存活率下降且造成細胞內鈣離子過量與活性氧化物（ROS）的增加。而在事先處理EGCG 30分鐘後則能減緩此傷害。EGCG也能透過活化肝糖合成酶激酶-3β（GSK-3β）/β-連環蛋白（β-catenin）/細胞週期蛋白D1（cyclin D1）的訊息傳遞路徑來取消雙氧水所造成的細胞週期停滯在G1-S階段。為了要了解EGCG在細胞膜表面的作用機制，我們將綠螢光蛋白（EGFP）異位地表現在H9c2細胞中。在表現EGFP的細胞中，隨著EGCG劑量的增加能誘導螢光強度發生變化，這表示EGCG的訊號傳遞能誘發EGFP鄰近的蛋白發生改變。透過蛋白鑑定的結果顯示與EGFP形成的複合體有67kD層黏連蛋白受體、窖蛋白-1與-3、β-肌動蛋白、肌凝蛋白-9和波形蛋白。透過表現EGFP的細胞與心肌梗塞的動物模式，我們發現窖蛋白參與EGCG保護心臟細胞的作用機轉。另外，利用蛋白質體分析鑑定出H9c2細胞在正常情況下、暴露在400μM的雙氧水30分鐘和事先處理20 μM EGCG 30分鐘再處理400μM的雙氧水30分鐘後蛋白間表現的差異。根據我們挑點的條件，共找出八個蛋白，分別與能量代謝、粒線體電子傳遞、氧化還原調節、訊息傳遞與RNA結合有關。此外，事先處理EGCG或GSK-3β抑制劑(SB216763)能減輕雙氧水所誘導的傷害，包括細胞存活率、磷酸化Akt（S473）和GSK-3β（S9）與cyclin D1蛋白的表現量。綜合來說，在雙氧水所誘導的氧化效應下，EGCG能增加AKT的活性是透過調節PIP3的合成，進而使導致心肌損傷的GSK-3β蛋白失去活性。

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