人體中每一秒鐘有數百萬個細胞進行生理性的細胞死亡，即細胞凋亡（apoptosis），所有的構造都需要至少一條路徑進行細胞凋亡來移除多餘或老化的細胞以維持組織器官的正常，其中粒線體在細胞凋亡的過程中也扮演著重要的角色。前列腺素為生物體其中的一種內分泌物，當細胞受到刺激而活化磷脂酶A2（phospholipase A2）時，細胞膜的磷脂質會被水解成花生四烯酸（arachidonic acid），再經由環氧合酵素（cyclooxygenase，COX）分解代謝成各種前列腺素（prostaglandins，PGs），如PGE2、PGF2α、PGD2、PGI2及TXA2。本研究使用NS-398，為COX-2的抑制劑，能抑制多種細胞株中COX-2的表現，同時也會引起細胞本身的細胞凋亡並抑制細胞的增殖生長，而不同劑量的NS-398對於A549細胞株的存活率也有不同的影響。前列腺素其訊息傳遞是經由細胞膜上的專一受體來傳達。依藥物刺激而產生不同的訊息傳遞途徑可將PGE2 receptor（EP receptor）分為四種不同的典型（EP1-EP4）以及一種PGF2α receptor（FP receptor）。實驗顯示在粒線體中有EP2、EP3及EP4的表現，而在細胞膜上有EP1、EP3、EP4及FP的表現。故在NS-398引起細胞凋亡的同時，可能是經由細胞膜或粒線體上受體表現程度的不同所導致的;實驗以EP2受體的促進劑及NS-398與A549細胞株共同培養，發現在50 μM濃度NS-398處理後，EP2受體的促進劑可以抑制細胞凋亡並增加細胞28 %的存活率。本實驗的結果顯示在NS-398所引起的細胞凋亡中，前列腺素可能是透過粒線體上受體的表現來引起訊息傳遞而影響細胞凋亡。

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