腺嘌呤核苷受体介导肿瘤坏死因子-α开放血肿瘤屏障的作用及其机制  

Adenosine receptor mediated effect and mechanism of tumor necrosis factor-α opening blood-tumor barrier

作　　者：秦丽娟[1] 谷艳婷[2] 王艳蕾[1] 张田[1] 贾永森[3] 王小君[1] 孙娜[1] 薛一雪[4] 

机构地区：[1]河北联合大学基础医学院,河北唐山063000 [2]沈阳药科大学生命科学与生物制药学院生理学教研室,辽宁沈阳110016 [3]河北联合大学中医学院,河北唐山063000 [4]中国医科大学基础医学院神经生物学教研室,辽宁沈阳110001

出　　处：《中国药理学通报》2013年第9期1248-1251,共4页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81101912);河北省卫生厅科学研究基金项目(No 20120144);国家教育部新教师基金项目(No 20102134120007);辽宁省博士启动基金项目(No 20101109)

摘　　要：目的明确肿瘤坏死因子-α(TNF-α)开放血肿瘤屏障的作用及其可能机制。方法构建体外血肿瘤屏障模型,给予TNF-α后不同时间点,免疫组织化学法和Western blot法动态检测胶质瘤细胞的热休克蛋白70(heat shock protein70,HSP70)和腺嘌呤核苷受体(adenosine A1receptor,A1R)的表达水平;荧光分析法检测体外血肿瘤屏障模型的通透性改变。结果给予TNF-α后,胶质瘤细胞内HSP70表达增加,于30 min时含量最多。C6细胞内A1R的表达水平也在给予TNF-α后明显增加,并于120 min达高峰后逐渐减少。其血肿瘤屏障的通透性亦于给予TNF-α后120 min达最大后减少。结论经TNF-α作用后的胶质瘤细胞HSP70表达增加,增加的HSP70可能是通过某种内在机制提高A1R的表达水平,进而增加了血肿瘤屏障的通透性。Aim To determine effect of tumor necrosis factor alpha （TNF alpha） opening blood tumor barrier and its possible mechanism. Methods Blood tumor barrier model was established in vitro, immunohisto- chemical and Western blot methods were used to detect dynamically heat shock protein 70 （HSPT0） and aden- osine A1 receptor（ AIR） expression levels in TNF al- pha treated glioma cells at different time points; Fluo- rescence analysis was adopted to test permeable chan- ges of blood tumor barrier model in vitro. Results HSP70 expression in glioma cells increased and reached peak content 30 min after TNF alpha was given in glioma cells. A1R expression level of C6 cells also increased and reached peak content 120 rain after TNF alpha was given and then gradually reduced. At the same time, the blood tumor barrier permeability also reached the peak. Conclusion HSP70 expression in glioma cells increases after TNF alpha treatment;the increased HSP70 might improve A1R expression level through an internal mechanism, and then increase the blood tumor barrier permeability.

关 键 词：TNF-α胶质瘤 血脑屏障 血肿瘤屏障 热休克蛋白 70 腺嘌呤核苷受体 

分 类 号：R341[医药卫生—基础医学] R342.4