中华预防医学杂志
中華預防醫學雜誌
중화예방의학잡지
CHINESE JOURNAL OF
2008年
6期
405-409
,共5页
丙烯腈%细胞增殖%细胞凋亡%大鼠%神经胶质细胞
丙烯腈%細胞增殖%細胞凋亡%大鼠%神經膠質細胞
병희정%세포증식%세포조망%대서%신경효질세포
Acrylonitrile%Cell proliferation%Apoptosis%Bats%Neurog]ia
目的 研究丙烯腈(acrylonitrile,ACN)对大鼠神经胶质正常细胞(DI TNC1)和大鼠神经胶质肿瘤细胞(C6细胞)的生长、凋亡、增殖及相关基因表达的影响.方法 ACN作用于DI TNC1和C6细胞的浓度是25、50和75μg/ml,对于细胞生长、凋亡和增殖实验,作用时间是24 h;对于微点阵(microarray)试验,作用时间分别是4、24 h.结果 25、50和75μg/ml ACN作用DI TNC1后,DNA合成指数降低,分别为对照的93.1%、81.3%和74.9%,细胞凋亡指数增加,分别为对照的118%、122%和143%;C6细胞的DNA合成指数和凋亡指数在ACN作用后基本没有变化;cyclin和p53等细胞增殖和凋亡相关基因的表达也有一定的变化.结论 ACN抑制了DI TNC1细胞的增殖和促进了其凋亡,对C6细胞的凋亡和增殖没有变化.
目的 研究丙烯腈(acrylonitrile,ACN)對大鼠神經膠質正常細胞(DI TNC1)和大鼠神經膠質腫瘤細胞(C6細胞)的生長、凋亡、增殖及相關基因錶達的影響.方法 ACN作用于DI TNC1和C6細胞的濃度是25、50和75μg/ml,對于細胞生長、凋亡和增殖實驗,作用時間是24 h;對于微點陣(microarray)試驗,作用時間分彆是4、24 h.結果 25、50和75μg/ml ACN作用DI TNC1後,DNA閤成指數降低,分彆為對照的93.1%、81.3%和74.9%,細胞凋亡指數增加,分彆為對照的118%、122%和143%;C6細胞的DNA閤成指數和凋亡指數在ACN作用後基本沒有變化;cyclin和p53等細胞增殖和凋亡相關基因的錶達也有一定的變化.結論 ACN抑製瞭DI TNC1細胞的增殖和促進瞭其凋亡,對C6細胞的凋亡和增殖沒有變化.
목적 연구병희정(acrylonitrile,ACN)대대서신경효질정상세포(DI TNC1)화대서신경효질종류세포(C6세포)적생장、조망、증식급상관기인표체적영향.방법 ACN작용우DI TNC1화C6세포적농도시25、50화75μg/ml,대우세포생장、조망화증식실험,작용시간시24 h;대우미점진(microarray)시험,작용시간분별시4、24 h.결과 25、50화75μg/ml ACN작용DI TNC1후,DNA합성지수강저,분별위대조적93.1%、81.3%화74.9%,세포조망지수증가,분별위대조적118%、122%화143%;C6세포적DNA합성지수화조망지수재ACN작용후기본몰유변화;cyclin화p53등세포증식화조망상관기인적표체야유일정적변화.결론 ACN억제료DI TNC1세포적증식화촉진료기조망,대C6세포적조망화증식몰유변화.
Objective To study the effect of acrylonitrile(CAN)to cell growth,apoptosis,proliferation and related gene expression of rat normal glial ceUs(DI TNCI)and tumor glial cells(C6).Methods The concentration of CAN on DI TNCI and C6 were 25,50 and 75μg/mL For cell growth,prolifcration and apoptosis assay,the treated time was 24 hours.for microarray assay,the treated time wa84 and 24 houm.Results After treatment of DI TNCl cell with 25,50 and 75μ/ml CAN,the DNA synthesis index were decreased 93.1%.81.3%and 74.9%as compared to control respectively,the apoptosis index Was increased 118%.122%and 143%as compared to controls respectively.The DNA syntllesis and apoptosis indexes of C6 cell showed no change after treatment with CAN.The cell cycle and apoptosis pathway related genes,such as cyclin and p53,also showed changes after treatment with AC N.Conclusion CAN inhibited the cell proliferation of DI TNCl.induced the apoptosis of DI TNCl and had no effect on cell proliferation and apoptosis of C6 cells,and the related regulation gene expression changes further confirmed the results.