CAJ | 학술논문

目的探索CCAAT增强子结合蛋白同源蛋白(CHOP)在丹参酮ⅡA(TanⅡA)诱导急性早幼粒细胞白血病(APL)细胞分化中的作用.方法反转录-聚合酶链反应(RT-PCR)及Western blot测定TanⅡA干预的NB4细胞的CHOP表达,通过形态学和膜表面标志检测APL细胞的分化,RNA干扰抑制CHOP表达.结果 TanⅡA诱导APL分化过程中伴有CHOP蛋白表达(1.933±0.987)和mRNA表达(1.587±0.815)的增加,相对于对照组蛋白和mRNA表达(0.537±0.110和0.713±0.090),差异有统计学意义(mRNA水平F=52.256,P＜0.01;蛋白水平F=114.852,P＜ 0.01)；TanⅡA联合RNA干扰抑制CHOP的表达能更加有效的提高APL的分化[(50.767±1.241)％与(16.167±2.122)％](F=989.431,P＜0.05)和凋亡[(89.233±5.581)％与(27.433±2.957)％](F=308.961,P＜0.05).结论 CHOP在Tan ⅡA诱导AtL分化过程中起着负向调节作用,抑制CHOP表达联合TanⅡA可能成为一个更好的治疗策略.
목적 탐색CCAAT증강자결합단백동원단백(CHOP)재단삼동ⅡA(TanⅡA)유도급성조유립세포백혈병(APL)세포분화중적작용.방법 반전록-취합매련반응(RT-PCR)급Western blot측정TanⅡA간예적NB4세포적CHOP표체,통과형태학화막표면표지검측APL세포적분화,RNA간우억제CHOP표체.결과 TanⅡA유도APL분화과정중반유CHOP단백표체(1.933±0.987)화mRNA표체(1.587±0.815)적증가,상대우대조조단백화mRNA표체(0.537±0.110화0.713±0.090),차이유통계학의의(mRNA수평F=52.256,P＜0.01;단백수평F=114.852,P＜ 0.01)；TanⅡA연합RNA간우억제CHOP적표체능경가유효적제고APL적분화[(50.767±1.241)％여(16.167±2.122)％](F=989.431,P＜0.05)화조망[(89.233±5.581)％여(27.433±2.957)％](F=308.961,P＜0.05).결론 CHOP재Tan ⅡA유도AtL분화과정중기착부향조절작용,억제CHOP표체연합TanⅡA가능성위일개경호적치료책략.
Objective To investigate the effect of CCAAT/enhancer-binding protein homologeus protein (CHOP) in Tan Ⅱ A treated acute promyelocytic leukemia (APL) cells.Methods APL cell differentiation was monitored by morphology and membrane differentiation antigens; expression of CHOP was inhibited by siCHOP; mRNA and protein expression of CHOP in Tan Ⅱ A-intervened APL cells were examined by RT-PCR and Western blot.Results Expression of CHOP was increased in Tan Ⅱ A induced differentiated APL cells (proteins levels 1.933±0.987 vs 0.537±0.110,F =114.852,P ＜ 0.01,mNRA levels 1.587±0.815 vs 0.713±0.090,F =52.256,P ＜ 0.01),combination of CHOP gene silencing with Tan Ⅱ A treatment induced strong APL cell differentiation [(50.767±1.241) ％ vs (16.167±2.122) ％,F =989.431,P ＜ 0.05] and apoptosis [(89.233±5.581) ％ vs (27.433±2.957) ％,F =308.961,P ＜ 0.05].Conclusion CHOP acts as a negative regulator in Tan Ⅱ A induced differentiation.Inhibition of CHOP may be a promising therapeutic strategy.