本文關鍵詞：地喹氯銨對腦膠質瘤細胞凋亡的影響　出處：《中國老年學雜志》2017年04期 　論文類型：期刊論文

  更多相關文章： 地喹氯銨 腦膠質瘤 增殖 凋亡 侵襲

【摘要】：目的探討地喹氯銨對腦膠質瘤細胞增殖、凋亡及侵襲的影響。方法用50、100、200μmol/L的地喹氯銨作用于腦膠質瘤細胞U251、U87、C6,作用時間分別為12、24、48、72、96 h,MTT檢測細胞增殖情況。流式細胞儀檢測76μmol/L的地喹氯銨作用48 h后的腦膠質瘤細胞U251的細胞凋亡情況。Transwell小室檢測地喹氯銨對腦膠質瘤細胞侵襲能力的影響。Western印跡檢測細胞中PI3K、p-PI3K、Akt、p-Akt蛋白的表達水平。結果 50、100、200μmol/L的地喹氯銨對U251、U87、C6腦膠質瘤細胞增殖均具有抑制作用。地喹氯銨對腦膠質瘤細胞的增殖抑制作用隨著作用時間的增加而增加,隨著藥物作用濃度的增加而增加。地喹氯銨作用膠質瘤U251、U87、C6細胞48 h的半數(shù)抑制濃度由大到小依次為:C6U87U251。76μmol/L的地喹氯銨作用后的腦膠質瘤細胞凋亡率明顯高于對照組(P0.01)。腦膠質瘤細胞經地喹氯銨作用后的侵襲細胞數(shù)明顯低于對照組(P0.01)。地喹氯銨作用后的腦膠質瘤細胞中PI3K、Akt的表達水平與對照組相比無明顯差異,而p-PI3K、p-Akt的表達水平明顯下降。結論地喹氯銨對腦膠質瘤細胞增殖、侵襲能力具有抑制作用,對腦膠質瘤細胞凋亡具有促進作用,作用機制與PI3K/Akt信號通路有關。
[Abstract]:Objective to investigate the effects of diammonium chloride on the proliferation, apoptosis and invasion of glioma cells. Methods 50,100,200 渭 mol/L of diammonium chloride was used to treat the glioma cell line U251 U87. The action time of C _ 6 was 12 ~ (24) C _ (24) O _ (48) C _ (2) H _ (72) ~ (96) h. MTT was used to detect cell proliferation. Flow cytometry was used to detect the action of dilqualkonium chloride at 76 渭 mol/L. Apoptosis of human glioma cell U251 after h .Transwell chamber assay of the effect of diammonium chloride on invasion of glioma cells. Western blot analysis of PI3 in human glioma cells. K. Results the expression level of p-PI3KCX AktPI3KGK and p-Akt protein was 50,100,200 渭 mol/L, and the expression level of p-PI3KT was 50,100,200 渭 mol/L on U251 U87. The proliferation of C6 glioma cells was inhibited, and the inhibitory effect of dilqualkonium chloride on the proliferation of glioma cells increased with the increase of the time of action. With the increase of drug action concentration, the glioma U251 U87 was induced by dilaquinamide. The apoptosis rate of glioma cells was significantly higher than that of the control group (P < 0.05). The half inhibitory concentration of C6 cells was higher than that of the control group (P < 0.05). The apoptosis rate of glioma cells was significantly higher than that of the control group (P < 0.01). The number of invasive cells in glioma cells treated with diqualone was significantly lower than that in the control group (P 0.01). The number of PI3K in glioma cells treated with diquinolium chloride was significantly lower than that in the control group. The expression level of Akt was not significantly different from that of the control group, but the expression level of p-PI3KN p-Akt was significantly decreased. Conclusion Diqualkonium chloride has an inhibitory effect on the proliferation and invasion of glioma cells. It can promote the apoptosis of glioma cells, and the mechanism is related to the PI3K/Akt signaling pathway.
【作者單位】： 錦州醫(yī)科大學藥學院;錦州醫(yī)科大學附屬第一醫(yī)院藥品管理科;
【基金】：遼寧省自然科學基金(No.2014022044)
【分類號】：R96
【正文快照】： 目前常用的治療腦膠質瘤的方法是手術治療和放療〔1〕,但由于腦膠質瘤具有發(fā)病隱匿、生長速度快、易轉移、易復發(fā)等特點,手術治療和放療效果仍然不理想。地喹氯銨(DECA)是一種廣譜抗菌藥,對分枝桿菌、革蘭陰性菌、革蘭陽性菌等具有抑制作用〔2〕,對口腔潰瘍、扁桃體炎、咽炎、

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