本文選題：氯通道　切入點：C1C-3　出處：《暨南大學》2011年碩士論文　論文類型：學位論文

【摘要】：目的：1)研究5-氟尿嘧啶(5-Fluorouacil,5-Fu)對低分化鼻咽癌細胞(CNE-2Z)凋亡的影響；2)5-Fu對CNE-2Z細胞氯通道的激活作用；3)氯通道在5-Fu誘導的CNE-2Z細胞凋亡性細胞容積減小和凋亡中的作用。 方法：1)Hoechst染色、流式細胞術分析細胞凋亡；2)Scion Image圖像分析軟件測量細胞直徑和面積,計算細胞標準容積；3)膜片鉗全細胞記錄技術記錄5-Fu激活的CNE-2Z細胞全細胞電流,計算電流密度。 結果： 1.5-Fu誘導CNE-2Z細胞產(chǎn)生明顯的細胞凋亡,100μmol/L 5-Fu作用48 h的凋亡率為(49.2±3.2)%,氯通道阻斷劑NPPB可使凋亡率下降至(12.5±2.6)%。 2.5-Fu誘導CNE-2Z細胞產(chǎn)生凋亡性細胞容積減小(Apoptotic volume decrease, AVD),胞外灌流100 umol/L 5-Fu 50 min細胞容積減小約9%,NPPB與5-Fu聯(lián)合作用相同時間細胞僅皺縮1.5%；氯通道阻斷劑明顯抑制5-Fu誘導的AVD。 3.5-Fu可以激活CNE-2Z細胞產(chǎn)生一個電流特征與容積激活性氯通道相似的氯電流；氯通道阻斷劑(NPPB, Tamoxifen)明顯抑制5-Fu激活的電流。 4. ClC-3SiRNA阻斷ClC-3氯通道表達,抑制5-Fu激活CNE-2Z細胞氯電流。 結論： 1.阻斷氯通道抑制5-Fu激活的CNE-2Z細胞氯電流,拮抗5-Fu誘發(fā)的凋亡性細胞容積減小和細胞凋亡等作用,提示氯通道在5-Fu誘導細胞凋亡中起重要作用。 2.ClC-3氯通道參與介導5-Fu激活的CNE-2Z細胞氯電流。
[Abstract]:Aim: to study the effect of 5-Fluorouaciline 5-Fu on apoptosis of poorly differentiated nasopharyngeal carcinoma (NPC) cell line CNE-2Z. The effect of 5-Fu on the activation of chloride channel in CNE-2Z cells and the role of chloride channel in 5-Fu induced apoptotic cell volume reduction and apoptosis of CNE-2Z cells were studied. Methods the cell diameters and area were measured by flow cytometry (FCM) and the cell diameter and area were measured by flow cytometry (FCM). The whole cell currents of 5-Fu activated CNE-2Z cells were recorded by patch clamp whole cell recording technique and the current density was calculated. Results:. 1. The apoptotic rate of CNE-2Z cells induced by 5-Fu was 49.2 鹵3.2 for 48 h, and the apoptosis rate decreased to 12.5 鹵2.6% by chloride channel blocker NPPB. 2.The volume of apoptotic cells in CNE-2Z cells induced by 5-Fu was reduced by Apoptotic volume decrease, AVDX, and extracellular perfusion of 100 umol/L 5-Fu 50 min cells. The cells only shrank at the same time after the combination of 5-Fu and 5-Fu, and the chloride channel blockers significantly inhibited 5-Fu induced AVDs. 3.5-Fu activated CNE-2Z cells to produce a chloride current similar to that of volume-activated chloride channel, and the chloride channel blocker NPPB( Tamoxifen) significantly inhibited the 5-Fu activated current. 4. ClC-3SiRNA blocked the expression of ClC-3 chloride channel and inhibited 5-Fu activation of chloride current in CNE-2Z cells. Conclusion:. 1. The blocking of chloride channel inhibits the chloride current of 5-Fu activated CNE-2Z cells, and antagonizes the effect of 5-Fu induced apoptosis on apoptotic cells, suggesting that chloride channel plays an important role in 5-Fu induced apoptosis. 2. ClC-3 chloride channel is involved in the regulation of chloride currents in 5-Fu activated CNE-2Z cells.
【學位授予單位】：暨南大學
【學位級別】：碩士
【學位授予年份】：2011
【分類號】：R739.63

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