本文選題：黃芩素　切入點：U　出處：《中國現(xiàn)代醫(yī)學(xué)雜志》2017年10期

【摘要】：目的探討黃芩素和U0126誘導(dǎo)人乳腺癌細(xì)胞株MCF-7凋亡的分子機(jī)制。方法單獨及聯(lián)合使用20μmol黃芩素、10μmol U0126處理MCF-7細(xì)胞24 h;光學(xué)顯微鏡觀察細(xì)胞數(shù)量變化,流式細(xì)胞術(shù)檢測MCF-7細(xì)胞周期變化,CCK8法檢測細(xì)胞增殖變化,TUNEL法和流式細(xì)胞術(shù)檢測細(xì)胞凋亡,實時聚合酶鏈反應(yīng)(Real Time PCR)和Western blot檢測凋亡相關(guān)因子m RNA和蛋白的表達(dá)水平。結(jié)果與黃芩素單獨刺激MCF-7細(xì)胞相比,黃芩素聯(lián)合U0126刺激MCF-7細(xì)胞時,S期細(xì)胞比例降低更明顯;MCF-7細(xì)胞經(jīng)不同濃度黃芩素或U0126處理后,增殖抑制,且具有濃度依賴性(P0.05);與黃芩素單獨處理MCF-7細(xì)胞相比,黃芩素與U0126聯(lián)合處理時,細(xì)胞凋亡更加顯著(P0.05),早期凋亡和晚期凋亡均增多(P0.05);與黃芩素或U0126單獨處理MCF-7細(xì)胞相比,黃芩素和U0126聯(lián)合處理MCF-7細(xì)胞時,凋亡抑制因子Bcl-2的m RNA水平降低(P0.05),凋亡促進(jìn)因子Bax的m RNA水平增高(P0.05),ERK1/2、GSK-3β和P38的磷酸化水平降低(P0.05),凋亡促進(jìn)因子Bax表達(dá)量增高(P0.05),凋亡抑制因子Bcl-2表達(dá)量降低(P0.05)。結(jié)論黃芩素或U0126通過調(diào)控Bcl-2/Bax的表達(dá)水平以及ERK1/2、GSK-3β和P38的磷酸化水平抑制MCF-7細(xì)胞增殖,促進(jìn)細(xì)胞凋亡,且具有協(xié)同效應(yīng)。因此,黃芩素和U0126可聯(lián)合用于臨床治療乳腺癌,具有重要臨床意義。
[Abstract]:Objective to investigate the molecular mechanism of baicalin and U0126 inducing apoptosis in human breast cancer cell line MCF-7. Methods MCF-7 cells were treated with 20 渭 mol baicalin 10 渭 mol U0126 for 24 h, and the number of MCF-7 cells was observed by optical microscope. MCF-7 cell cycle changes were detected by flow cytometry. Cell proliferation was detected by CCK8 method and apoptosis was detected by Tunel and flow cytometry. Real-time polymerase chain reaction (Time) and Western blot were used to detect the expression of apoptosis-related factor m RNA and protein. Results compared with baicalin alone, the expression of m RNA and protein was detected in MCF-7 cells. The ratio of S phase cells in MCF-7 cells stimulated by baicalin combined with U0126 was significantly decreased after treated with different concentrations of baicalin or U0126, the proliferation of MCF-7 cells was inhibited in a concentration-dependent manner, compared with that of MCF-7 cells treated with baicalin alone. When combined with baicalin and U0126, the apoptosis of MCF-7 cells was significantly higher than that of baicalein and U0126, and increased in both early and late stages of apoptosis. Compared with baicalin or U0126 alone, baicalein and U0126 treated MCF-7 cells. The level of m RNA of apoptosis inhibitor Bcl-2 decreased P0.05, the level of m RNA of Bax increased and the phosphorylation of P0.05 / ERK1 / 2 + GSK-3 尾 and P38 decreased, the expression of Bax increased and Bcl-2 decreased P0.055.Conclusion the expression of Bcl-2 is lower than that of Bax. Baicalin or U0126 inhibited the proliferation of MCF-7 cells by regulating the expression of Bcl-2/Bax and phosphorylation of ERK1 / 2, GSK-3 尾 and P38. The combination of baicalin and U0126 can be used in clinical treatment of breast cancer and has important clinical significance.
【作者單位】： 四川省瀘州市人民醫(yī)院乳腺外科;西南醫(yī)科大學(xué)附屬中醫(yī)醫(yī)院婦產(chǎn)科;西南醫(yī)科大學(xué)附屬醫(yī)院醫(yī)學(xué)實驗中心;西南醫(yī)科大學(xué)附屬醫(yī)院婦產(chǎn)科;西南醫(yī)科大學(xué)醫(yī)學(xué)信息與工程學(xué)院;
【基金】：四川省科技廳項目(14JC01353-LH67) 四川省瀘州市科技局項目(2014-S-44)
【分類號】：R737.9

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