中华消化杂志
中華消化雜誌
중화소화잡지
Chinese Journal of Digestion
2011年
7期
474-478
,共5页
覃林花%吕礁%施云星%周国中%季兴英%李琳%郭亚军%卫立辛
覃林花%呂礁%施雲星%週國中%季興英%李琳%郭亞軍%衛立辛
담림화%려초%시운성%주국중%계흥영%리림%곽아군%위립신
趋化因子CCL3%4-1BB配体%癌,肝细胞%疾病模型,动物%存活率
趨化因子CCL3%4-1BB配體%癌,肝細胞%疾病模型,動物%存活率
추화인자CCL3%4-1BB배체%암,간세포%질병모형,동물%존활솔
Chemokine CCL3%4-1BB Ligand%Carcinoma,hepatocellular%Disease models,animal%Survival rate
目的 观察巨噬细胞炎性蛋白-1α(MIP-1α)联合4-1BB配体(4-1BB L)对肝癌细胞体内致瘤性的影响.方法 以小鼠4-1BB L(m4-1BB L)重组逆转录病毒感染Hepa 1-6小鼠MIP-1α(mMIP-1α),筛选并扩增抗性克隆,以流式细胞术检测m4-1BB L的表达,绘制并比较mMIP-1α和m4-1BB L同时或单独表达的Hepa 1-6细胞的生长曲线.C57B/L小鼠随机分为7组,每组9只,各组分别接种Hepa 1-6 mMIP-1α+m4-1BB L、Hepa 1-6 m4-1BB L、Hepa 1-6 mMIP-1α、Hepa 1-6 pBabe puro、Hepa 1-6、Hepa 1-6 pLXSHD和PBS,观察比较各组肝癌细胞的致瘤性,比较各组小鼠的存活率.结果 成功获得同时表达mMIP-1α和m4-1BB L的小鼠肝癌细胞Hepa 1-6 mMIP-1α+m4-1BB L,mMIP-1α和m4-1BB L同时或单独表达不影响Hepa 1-6的生长曲线.观察5周,Hepa 1-6 mMIP-1α+m4-1BB L接种的小鼠均未生长肿瘤,Hepa 1-6 mMIP-1α+m4-1BB L的体内致瘤性低于Hepa 1-6 mMIP-1α和Hepa 1-6 m4-1BB L.接种Hepa 1-6 mMIP-1α+m4-1BBL的小鼠12周末存活率(9/9)高于接种Hepa 1-6 m4-1 BB L小鼠(6/9)和Hepa 1-6 mMIP-1α小鼠(1/9).结论 趋化因子MIP-1α联合共刺激分子4-1BB L降低了肝癌细胞体内致瘤性,并使小鼠的生存期延长.
目的 觀察巨噬細胞炎性蛋白-1α(MIP-1α)聯閤4-1BB配體(4-1BB L)對肝癌細胞體內緻瘤性的影響.方法 以小鼠4-1BB L(m4-1BB L)重組逆轉錄病毒感染Hepa 1-6小鼠MIP-1α(mMIP-1α),篩選併擴增抗性剋隆,以流式細胞術檢測m4-1BB L的錶達,繪製併比較mMIP-1α和m4-1BB L同時或單獨錶達的Hepa 1-6細胞的生長麯線.C57B/L小鼠隨機分為7組,每組9隻,各組分彆接種Hepa 1-6 mMIP-1α+m4-1BB L、Hepa 1-6 m4-1BB L、Hepa 1-6 mMIP-1α、Hepa 1-6 pBabe puro、Hepa 1-6、Hepa 1-6 pLXSHD和PBS,觀察比較各組肝癌細胞的緻瘤性,比較各組小鼠的存活率.結果 成功穫得同時錶達mMIP-1α和m4-1BB L的小鼠肝癌細胞Hepa 1-6 mMIP-1α+m4-1BB L,mMIP-1α和m4-1BB L同時或單獨錶達不影響Hepa 1-6的生長麯線.觀察5週,Hepa 1-6 mMIP-1α+m4-1BB L接種的小鼠均未生長腫瘤,Hepa 1-6 mMIP-1α+m4-1BB L的體內緻瘤性低于Hepa 1-6 mMIP-1α和Hepa 1-6 m4-1BB L.接種Hepa 1-6 mMIP-1α+m4-1BBL的小鼠12週末存活率(9/9)高于接種Hepa 1-6 m4-1 BB L小鼠(6/9)和Hepa 1-6 mMIP-1α小鼠(1/9).結論 趨化因子MIP-1α聯閤共刺激分子4-1BB L降低瞭肝癌細胞體內緻瘤性,併使小鼠的生存期延長.
목적 관찰거서세포염성단백-1α(MIP-1α)연합4-1BB배체(4-1BB L)대간암세포체내치류성적영향.방법 이소서4-1BB L(m4-1BB L)중조역전록병독감염Hepa 1-6소서MIP-1α(mMIP-1α),사선병확증항성극륭,이류식세포술검측m4-1BB L적표체,회제병비교mMIP-1α화m4-1BB L동시혹단독표체적Hepa 1-6세포적생장곡선.C57B/L소서수궤분위7조,매조9지,각조분별접충Hepa 1-6 mMIP-1α+m4-1BB L、Hepa 1-6 m4-1BB L、Hepa 1-6 mMIP-1α、Hepa 1-6 pBabe puro、Hepa 1-6、Hepa 1-6 pLXSHD화PBS,관찰비교각조간암세포적치류성,비교각조소서적존활솔.결과 성공획득동시표체mMIP-1α화m4-1BB L적소서간암세포Hepa 1-6 mMIP-1α+m4-1BB L,mMIP-1α화m4-1BB L동시혹단독표체불영향Hepa 1-6적생장곡선.관찰5주,Hepa 1-6 mMIP-1α+m4-1BB L접충적소서균미생장종류,Hepa 1-6 mMIP-1α+m4-1BB L적체내치류성저우Hepa 1-6 mMIP-1α화Hepa 1-6 m4-1BB L.접충Hepa 1-6 mMIP-1α+m4-1BBL적소서12주말존활솔(9/9)고우접충Hepa 1-6 m4-1 BB L소서(6/9)화Hepa 1-6 mMIP-1α소서(1/9).결론 추화인자MIP-1α연합공자격분자4-1BB L강저료간암세포체내치류성,병사소서적생존기연장.
Objective To investigate the effects of macrophage inflammatory protein-1α (MIP-1α) combined with molecule 4-1BB L on the tumorigenicity of hepatocellular carcinoma cells in vivo. Methods Mouse MIP-1α (mMIP-1α) expressed Hepa 1-6 cells were transfected with m4-1BBL recombinant retrovirus, the anti-histidinol cells clones were selected and amplified. The expression of m4-1BB L was confirmed by flow cytometry. The growth curve of Hepa 1-6 cells transfected with mMIP-1α and m4-1BBL alone or together was drawn and compared. C57B/L Mice were randomly divided into 7 groups, 9 mice in each group, injected with mMIP-1α+m4-1BB L Hepa 1-6 cells, m4-1BB L Hepa 1-6 cells, mMIP-1α Hepa 1-6 cells, Hepa 1-6 cells, pLXSHD Hepa 1-6 cells or PBS respectively. The tumorigenicity of hepatocellular carcinoma cells and the mice survival rate were compared between each groups. Results Hepa 1-6 mMIP-1α+m4-1BB L cells which expressed both mMIP-1α and m4-1BB L were successfully established. The expression of mMIP-1α and m4-1BB L alone or together did not affect the growth curve of Hepa 1-6 cells. Observed for 5 weeks, no tumor developed in Hepa 1-6 mMIP-1α+m4-1BB L injected mice. The tumorigenicity of Hepa 1-6 mMIP-1α+m4-1BB L was lower than that of Hepa 1-6 mMIP-1α or Hepa 1-6 m4-1BB L in vivo. The survival rate of Hepa 1-6 mMIP-1α+m4-1BBL injected mice(9/9) was higher than that of Hepa 1-6 m4-1BB L injected mice (6/9)or Hepa 1-6 mMIP-1α injected mice (1/9). Conclusion Chemokine MIP-1α combined with costimulatory 4-1BB L lowered the tumorigenicity of hepatocellular carcinoma cells in vivo, and prolonged the mice survival period.