TNF-α在热疗降低胶质瘤侵袭性过程中的作用

 目的 探讨肿瘤坏死因子-α(TNF-α)在热疗抑制肿瘤侵袭性过程中的作用。方法 热处理大鼠恶性胶质瘤细胞(C6细胞)和胶质瘤大鼠后，放射免疫法监测培养液和脑胶质瘤组织内TNF-α的浓度；免疫组化法检测经热疗/ TNF-α/生理盐水处理过的胶质瘤组织内增殖细胞核抗原(PCNA)蛋白的表达。利用Transwell构建肿瘤侵袭模型，通过结晶紫染色法检测肿瘤侵袭性。电镜观察C6恶性胶质瘤大鼠肿瘤血管内皮细胞的凋亡。结果 热疗可增加C6细胞培养液和胶质瘤大鼠肿瘤组织内的TNF-α含量及降低胶质瘤侵袭性，均于热疗后120min时达高峰(P＜0.01)。热疗与TNF-α单独作用于胶质瘤大鼠后，均可引起胶质瘤大鼠肿瘤血管内皮细胞的凋亡。且TNF-α引起内皮细胞的凋亡水平与热处理后C6细胞培养液中TNF-α含量一致。结论 热疗可能是通过增加TNF-α引起肿瘤血管内皮细胞凋亡而抑制了肿瘤侵袭性。

Hyperthermia-induced glioma invasiveness decrease is mediated by tumor necrosis factor-alpha

Objective Role of tumor necrosis factor-α(TNF-α) during hyperthermia- induced tumor invasiveness decreases process. Methods Immunohistochemical method detect proliferating cell nuclear antigen(PCNA) of glioma tissue treated by hyperthemia/TNF-α/normal saline(NS), radioimmunoassay monitoring TNF-α content of culture medium and brain glioma tissue after heat treated tumor-bearing rat and rat glioma cell line (C6 cell). Established a tumor model using Transwell, crystal violet staining determine tumor invasiveness. Electron microscope of tumor vascular endothelial cell apoptosis. Results Hyperthemia not only increased the content of TNF-α of C6 rat glioma cell culture medium and tumor tissue, but also decreased glioma invasiveness. Both reached the peak at 120 minute after hyperthermia(P＜0.01). Hyperthemia and TNF-α used respectively on the tumor-bearing rats, all can caused apoptosis of tumor vasculature endothelial cells. TNF-α caused tumor vascular endothelial cell apoptosis levels had the same trend with TNF-α content of C6 cell culture fluid after hyperthemia. Conclusion Hyperthemia induced tumor vascular endothelial cell apoptosis and inhibit tumor invasiveness may be to increased TNF-α content in tumor tissue.