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肿瘤坏死因子相关凋亡诱导配体诱导人脑胶质瘤细胞凋亡作用的研究 被引量:2

Study of apoptosis induced by TRAIL in human glioma cells
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摘要 目的研究肿瘤坏死因子相关凋亡诱导配体(TRAIL)受体在不同级别胶质瘤中的表达及TRAIL对原代培养的胶质瘤细胞凋亡的诱导作用.方法应用原位杂交的方法检测TRAIL受体在45例胶质瘤和5例正常脑组织中的转录表达;分别对其中22例和3例进行原代培养,用流式细胞仪检测TRAIL作用后细胞的凋亡率.结果在45例胶质瘤中,DR4、DR5、DcR1、DcR2的mRNA的表达例数分别为38例、41例、40例、2例.成功培养出18例胶质瘤细胞和3例正常胶质细胞, TRAIL作用后凋亡率在80%以上、50%~80%、50%以下的例数分别为5例、9例、4例,正常胶质细胞无明显凋亡发生.结论 TRAIL受体的表达与肿瘤的恶性程度无关;TRAIL能有效地选择性杀死胶质瘤细胞. Objective To study the expression of TRAIL receptors in gliomas of different grades,and the apoptosis induced by TRAIL in primary culture cells of human gliomas. Methods The mRNA of TRAIL receptors in 45 specimens of surgically resected gliomas and 5 normal cerebral tissue specimens was detected by hybridization in situ. Primary culture was carried out in 22 gliomas and 3 normal cerebral tissue specimens,and then the apoptosis of glioma cells and normal glialcells induced by TRAIL was assayed by flow cytometry. Results Of 45 gliomas,the expressions of DR4, DR5,DcR1 and DcR2 were found in 38 cases,41 cases.40 cases and 2 cases respectively. 18 cases of glioma cells and 3 cases of normal glial cells were successfully cultured,the apoptotic rate which was above 80 % , between 50 % - 80 % and below 50 % was found in 5 cases, 9 cases and 4 cases respectively after application TRAIL,normal glial cells had no obvious apoptosis. Conclusions Expression of TRAIL receptors is not correlated with the malignant degree of gllomas. TRAIL can induce apoptosis in certain glioma cells effectively and selectively.
出处 《中国基层医药》 CAS 2005年第10期1311-1313,共3页 Chinese Journal of Primary Medicine and Pharmacy
关键词 胶质瘤 细胞凋亡 原位杂交 流式细胞术 肿瘤坏死因子相关凋亡诱导配体 人脑胶质瘤细胞 凋亡作用 TRAIL受体 流式细胞仪检测 原代培养 Glioma Apoptosis In situ hybridization Flow cytometry TNF- related apoptosis inducing ligand
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  • 2Ashkenazi A,Pai RC,Fong S,et al.Safty and antitumor activity of recombinant soluble Apo2 ligand.J Cli Invest,1999,104:155-162.
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  • 4Rohn TA,Wagenknecht B,Roth W,et al.CCNU-dependent potentiation of TRAIL/Apo2L-induced apoptosis in human glioma cells is p53-independent but may involve enhanced cytochrome c release.Oncogene,2001,20:4128-4137.
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