CAJ | 학술논문

目的：探讨肿瘤坏死因子-α( tumor necrosis factor-α, TNF-α)在替莫唑胺( temozolomide, TMZ)降低胶质瘤侵袭性过程中的作用及机制。方法对数生长期的C6胶质瘤细胞随机分为TMZ处理10、30、60、120、180和240 min组,每组各15例,动态监测培养液中TNF-α的含量(放射免疫法)、C6细胞内 p53蛋白的表达( Western blot法)和细胞凋亡水平( AnnexinV-FITC法)。制备体外胶质瘤的侵袭模型,利用结晶紫染色法检测胶质瘤的侵袭性。结果 TMZ作用于C6细胞后,培养液中TNF-α的含量明显增加,于120 min时含量最多(P<0．01),其后开始减少。 C6细胞内p53蛋白的表达于处理后120 min达高峰(P<0．01),其后逐渐减少。 TMZ作用于体外胶质瘤侵袭模型后,胶质瘤细胞的侵袭性降低。结论 TNF-α介导TMZ降低胶质瘤侵袭性,此作用可能是由于TMZ促进C6细胞释放TNF-α,增加的TNF-α又促进胶质瘤细胞凋亡所致。
목적：탐토종류배사인자-α( tumor necrosis factor-α, TNF-α)재체막서알( temozolomide, TMZ)강저효질류침습성과정중적작용급궤제。방법대수생장기적C6효질류세포수궤분위TMZ처리10、30、60、120、180화240 min조,매조각15례,동태감측배양액중TNF-α적함량(방사면역법)、C6세포내 p53단백적표체( Western blot법)화세포조망수평( AnnexinV-FITC법)。제비체외효질류적침습모형,이용결정자염색법검측효질류적침습성。결과 TMZ작용우C6세포후,배양액중TNF-α적함량명현증가,우120 min시함량최다(P<0．01),기후개시감소。 C6세포내p53단백적표체우처리후120 min체고봉(P<0．01),기후축점감소。 TMZ작용우체외효질류침습모형후,효질류세포적침습성강저。결론 TNF-α개도TMZ강저효질류침습성,차작용가능시유우TMZ촉진C6세포석방TNF-α,증가적TNF-α우촉진효질류세포조망소치。
Purpose To explore the role of tumor necrosis factor-α( TNF-α) in the process of temozolomide ( TMZ) reduce glioma in-vasiveness and its possible mechanism. Methods C6 glioma cells of logarithmic phase were randomly divided into TMZ treatment (10, 30, 60, 120, 180, 240 min group) (n=15), dynamic monitoring content of TNF-αin the culture medium was measured by ra-dioimmunoassay, expression of p53 protein in C6 cells was detected with Western blotting method, and cell apoptosis was used with AnnexinV-FITC. A glioma invasiveness model was established in vitro and glioma invasiveness was determined by crystal violet stai-ning. Results For C6 cells, contents of TNF-αin the nutrient fluid and expressions of p53 protein in C6 cells obviously increased af-ter TMZ treatment and they achieved the peak at 120 min (P<0. 01), followed by decrease gradually. Glioma invasiveness was re-duced after TMZ acted on glioma in vitro. Conclusion TMZ can reduce glioma invasiveness by TNF-α, which this role may be is TMZ promote C6 cells release of TNF-α and increased TNF-α due to glioma cells apoptosis.