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共固定化细胞因子诱导的HeLa细胞凋亡中Bax、Bcl-2、P53基因的表达

Expression of Bax,Bcl-2 and P53 in the HeLa Apoptosis Induced by Co-immobilized Cytokines

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【作者】 关燕清邱李莉王文文

【Author】 Guan Yanqing Qiu Lili Wang Wenwen(College of Life Science,South China Normal University,Guangzhou 510631,China)

【机构】 华南师范大学生命科学学院

【摘要】 我们研究了游离药物与共固定药物作用后HeLa细胞的Bax、Bcl-2和P53基因蛋白的表达变化。人子宫颈癌细胞系(HeLa细胞)经过游离和共固定两种药物分别作用24、72、120、168 h后,用免疫组织化学的方法检测Bax、Bcl-2和P53基因蛋白表达,经图像分析仪检测反应产物的光密度并进行统计分析。发现两种药物作用120 h后的Bcl-2的平均光密度明显降低,而Bax的平均光密度明显上升,P53随着时间的延长平均光密度也随之升高;共固定药物在120 h后Bax/Bcl-2的比值明显比游离药物高。研究表明,干扰素和肿瘤坏死因子共同作用HeLa细胞,P53表达上调诱导Bax基因表达、抑制Bcl-2基因的表达,很有可能是通过线粒体通路诱导细胞凋亡。

【Abstract】 The aim of this study was to evaluate the changes in the expression of Bax,Bcl-2 and P53 when HeLa cells were induced by free cytokines or co-immobilized cytokines.The cells were induced for 24hrs,72hrs,120hrs and 168hrs.Then,the expression of Bax,Bcl-2 and P53 was observed by immunohistochemistry.The average optic density of reaction products was tested by image analysis.Lastly,data were analyzed statistically.After the HeLa cells were induced for 120hrs, the average optic denisity of Bcl-2 was much decreased.However,the average optic Bax was much increased.The average optic density of P53 also increased with the increase of time.The results suggest that HeLa apoptosis was induced by tumor necrosis factor-α and interferon-γ,and the increasing expression of P53 may induce the expression of Bax and prevent the expression of Bcl-2,via the mitochondrial induction of cell apoptosis.

【基金】 广东省科技项目资助(2006B35802003)
  • 【文献出处】 生物医学工程学杂志 ,Journal of Biomedical Engineering , 编辑部邮箱 ,2009年01期
  • 【分类号】R737.33
  • 【被引频次】4
  • 【下载频次】307
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