摘要
目的:探讨肿瘤坏死因子-α(TNF-α)在缓激肽(BK)开放血肿瘤屏障(BTB)过程中的作用。方法:缓激肽处理C6细胞和胶质瘤大鼠后,放射免疫法动态监测培养液和脑胶质瘤组织内TNF-α浓度。利用伊文思蓝连续监测缓激肽/TNF-α处理后的C6恶性胶质瘤大鼠血肿瘤屏障的通透性,同时电镜观察血肿瘤屏障的病理学改变。结果:缓激肽可增加C6细胞培养液和胶质瘤大鼠肿瘤组织内的TNF-α含量,且两者均于给予缓激肽后15min时达高峰(与对照组相比有显著统计学意义,P<0.01)。TNF-α与缓激肽单独作用于C6动物后,均可引起胶质瘤大鼠的血肿瘤屏障紧密连接开放及通透性增加。且肿瘤坏死因子-α对肿瘤模型动物血肿瘤屏障通透性的影响与C6细胞培养液中TNF-α含量相一致。结论:缓激肽开放血肿瘤屏障过程中,可能是通过某种机制引起肿瘤组织内TNF-α增加,增加的TNF-α进而引起了血肿瘤屏障的开放。
Objective To investigate the role of tumor necrosis factor-alpha （TNF-α） play in the opening of blood-tumor barrier （BTB） by bradykinin. Methods C6 cells and rats with glioma were administered with bradykinin, then the contents of TNF-α in the culture fluid of C6 cells and glioma tissues were measured by radioimmunoassay. The permeability and pathology of BTB in rats after bradykinin administration were observed by Evans blue （EB） and electron microscopy. Results The contents of TNF-α were obviously increased in the culture fluid of C6 cells and glioma tissues （as compared with control group, P 〈 0.01） after bradykinin administration, and reached their peak 15 rain later. The tight junction of BTB was opened and the permeability was increased in rats administered with bradykinin. The effect of TNF-α on the permeability of BTB in rats were similar to that in the culture fluid. Conclusion The opening of BTB by bradykinin may mediated by the increase of TNF-α
出处
《实用医学杂志》
CAS
北大核心
2012年第6期899-902,共4页
The Journal of Practical Medicine
基金
国家自然科学基金资助项目(编号:81101912)
河北省卫生厅科研基金项目(编号:20100464
20110165)
河北联合大学博士启动基金项目(编号:BS09012)
河北联合大学大学生创新性实验计划项目(编号:X2011035)
国家教育部新教师基金项目(编号:20102134120007)
辽宁省博士启动基金项目(编号:20101109)
唐山市科学技术研究与发展计划项目(编号:1113020486)
关键词
肿瘤坏死因子-Α
缓激肽
血肿瘤屏障
Tumor necrosis factor-alpha
Bradykinin
Blood-tumor barrier
