本文選題：血液腫瘤 + 骨髓微環(huán)境�。� 參考：《華中科技大學(xué)學(xué)報(bào)(醫(yī)學(xué)版)》2017年04期

【摘要】：目的探討骨髓基質(zhì)細(xì)胞通過上調(diào)纖維連接蛋白介導(dǎo)白血病Jurkat細(xì)胞化療耐藥。方法使用CCK-8法檢測白血病Jurkat細(xì)胞對(duì)化療藥物吡柔比星的敏感性,繪制敏感曲線;體外建立Jurkat細(xì)胞與骨髓基質(zhì)細(xì)胞(BMSC)共培養(yǎng)接觸耐藥模型,檢測該模型中在吡柔比星作用下Jurkat細(xì)胞的抑制率,并檢測在該模型中纖維連接蛋白(FN)的表達(dá)水平;體外建立Jurkat細(xì)胞與FN作用的粘附耐藥模型,檢測該模型中在吡柔比星作用下Jurkat細(xì)胞的抑制率;使用流式細(xì)胞儀檢測在BMSC/FN耐藥模型及單獨(dú)培養(yǎng)模型中Jurkat細(xì)胞在吡柔比星作用下的凋亡率;收集復(fù)發(fā)難治血液腫瘤患者及正常人骨髓標(biāo)本,檢測標(biāo)本上清中FN的水平。結(jié)果在與BMSC共培養(yǎng)接觸耐藥模型中,在相同濃度吡柔比星作用下,在同一時(shí)間點(diǎn),Jurkat細(xì)胞凋亡率較單獨(dú)培養(yǎng)組明顯下降。在Jurkat細(xì)胞與BMSC共培養(yǎng)的接觸耐藥模型中,上清中分泌的FN明顯上升。在FN作用的粘附耐藥模型中,在相同濃度吡柔比星作用下,在同一時(shí)間點(diǎn),Jurkat細(xì)胞凋亡率較單獨(dú)培養(yǎng)組明顯下降。與正常人比較,復(fù)發(fā)難治血液腫瘤患者骨髓上清中檢測的FN水平明顯上升。結(jié)論復(fù)發(fā)難治血液腫瘤患者的骨髓中,FN分泌增加;通過體外共培養(yǎng)模型提示骨髓基質(zhì)細(xì)胞可以分泌FN,介導(dǎo)白血病Jurkat細(xì)胞發(fā)生化療耐藥,推測在白血病患者的骨髓微環(huán)境中,基質(zhì)細(xì)胞可以為白血病細(xì)胞在化療中提供耐藥支持,黏附分子FN可能參與其中,是介導(dǎo)白血病細(xì)胞化療耐藥的重要原因。
[Abstract]:Objective to investigate the chemotherapeutic resistance of leukemic Jurkat cells mediated by bone marrow stromal cells up-regulated by fibronectin. Methods CCK-8 assay was used to detect the sensitivity of leukemia Jurkat cells to the chemotherapeutic drug pirarubicin and to draw a sensitive curve. The contact resistance model of Jurkat cells and bone marrow stromal cells (BMSCs) was established in vitro. The inhibition rate of Jurkat cells and the expression of fibronectin (FN) in the model were detected, and the adhesion resistance model of Jurkat cells to FN was established in vitro. The inhibition rate of Jurkat cells under the action of pirarubicin and the apoptosis rate of Jurkat cells under the action of pirarubicin in BMSC/FN resistant model and single culture model were detected by flow cytometry. Bone marrow samples were collected from patients with refractory hematological tumors and normal controls. FN levels in the supernatants were measured. Results in the model of drug resistance in co-culture with BMSC, the apoptosis rate of Jurkat cells in the same concentration of pirarubicin was significantly lower than that in the single culture group at the same time. In the contact resistant model of Jurkat cells co-cultured with BMSC, FN secreted in the supernatant increased significantly. In the model of adhesion resistance induced by FN, the apoptotic rate of Jurkat cells at the same time point in the same concentration of pirarubicin was significantly lower than that in the single culture group. The level of FN in bone marrow supernatant of patients with recurrent and refractory hematoma was significantly higher than that of normal controls. Conclusion the results suggest that bone marrow stromal cells can secrete FNs and mediate chemotherapeutic resistance of leukemic Jurkat cells in the bone marrow microenvironment of leukemia patients. Stromal cells can provide chemotherapeutic support for leukemia cells, and adhesion molecule FN may be involved in it, which is an important reason for the chemotherapeutic resistance of leukemia cells.
【作者單位】： 湖北省腫瘤醫(yī)院腫瘤內(nèi)科;武漢市第五醫(yī)院腫瘤科;華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院血液科;
【基金】：國家自然科學(xué)基金資助項(xiàng)目(No.30770913)
【分類號(hào)】：R733.7

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 羅麗;骨髓基質(zhì)細(xì)胞與凋亡[J];中國局解手術(shù)學(xué)雜志;2002年04期

2 劉耀;張曦;司英健;高蕾;高力;陳幸華;;急性淋巴細(xì)胞白血病骨髓基質(zhì)細(xì)胞縫隙連接功能的研究[J];醫(yī)學(xué)研究生學(xué)報(bào);2007年04期

3 王歡;周s，

本文編號(hào)：1828294