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Activation of Protein Expression in Clonal Glioma Cells by Sodium Butyrate

丁酸鈉誘發神經膠瘤細胞蛋白質表現之研究

摘要


丁酸鈉對神經膠瘤細胞之異常增殖行為有極顯著的抑制效果。同時,這些丁酸鈉處理所造成之影響皆為可逆性。經丁酸鈉處理後之神經膠瘤細胞其DNA銳減,惟細胞內蛋白質卻有明顯蓄積現象。若以SDS-PAGE法分析,亦可見多種蛋白質之含量普遍皆有昇高的趨勢,亦可見多種蛋白質之含量普遍皆有昇高的趨勢,尤其是BIP1、BIP2、BIP3與BIP4等蛋白質有極顯著的增加;其中BIP4蛋白質之變化僅在接受丁酸鈉處理之細胞質發現,但是BIP1、BIP2與BIP3因丁酸納處理而發生之變化雖然主要存在於細胞質內,然而於細胞核中亦可發現類似的改變。若以35S-me-thionine分析丁酸鈉處理之神經膠細胞所合成的蛋白質,可見BIP1、BIP2、BIP3與BIP4四種蛋白質之合成皆明顯地增加。利用雙向電泳法分析之結果顯示:丁酸鈉之處理促使細胞內鹼性蛋白質減少;此外,分子量為100Kda之蛋白質,其PI值原為6.66,經丁酸鈉處理後卻轉移至6.72之位置。 綜合上述得知(1)丁酸鈉對神經膠瘤細胞之異常增殖現象有極顯著的抑制效果,並旦能促使此腫瘤細胞發生生化方面之分化。(2)可酸鈉能誘發神經膠瘤細胞內蛋白質的合成增加,而促使細胞內的蛋白質產生不同的表現方式。

關鍵字

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並列摘要


Butyrate exerts a potent inhibitory effect on the proliferation of anaplastic glioma cells. Following exposure to 2.5 mM sodium butyrate, the growth rate of clonal glioma cells was markedly reduced. The cellular DNA content of glioma cells was significantly reduced as a result of butyrate exposure, while the cellular protein content of butyrate-treated glioma cells increased considerably. Analyses with SDS-polyacrylamide gel electrophoresis of proteins derived from butyrate-treated glioma revealed that BIP1,BIP2 and BIP3 increased significantly in quantities, which could be found in nuclear fraction and cytoplasmic fraction simultaneously. But BIP4, which was also enhanced markedly, was found only in the cytoplasmic fraction. The incorporation of 35S-methionine into BIP1, BIP2, BIP3 and BIP4 was virtually increased after the treatment with butyrate for 48 hours. Additional results obtained with two-dimensional gel electrophoresis indicated that the pI value of protein (100 KDa)was shifted from 6.66 to 6.72 following butyrate exposure. The conclusions derived are as following: (1) Butyrate is a potent, reversible inhibitory agent in the proliferation of glioma cells. (2) Butyrate is capable of activating the protein expression by way ofincreasing in protein synthesis.

並列關鍵字

butyrate glioma cells

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