中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2013年
1期
24-27
,共4页
高崇崇%巩本刚%夏修良%宋德坤%徐怀勇
高崇崇%鞏本剛%夏脩良%宋德坤%徐懷勇
고숭숭%공본강%하수량%송덕곤%서부용
胰腺肿瘤%MMI-166%金属蛋白酶类组织抑制剂%细胞凋亡
胰腺腫瘤%MMI-166%金屬蛋白酶類組織抑製劑%細胞凋亡
이선종류%MMI-166%금속단백매류조직억제제%세포조망
Pancreatic neoplasm%MMI-166%Tissue inhibitor of metalloproteinases%Apoptosis
目的 观察MMI-166对人胰腺癌SW1990细胞及其移植瘤组织凋亡相关蛋白表达的影响,探讨其可能机制.方法 应用人胰腺癌细胞株SW1990建立裸鼠胰腺癌皮下移植瘤模型,按完全随机法将荷瘤裸鼠分为对照组和MMI-166组,分别给予口服生理盐水和MMI-166(200 mg·kg-1·d-1),持续28 d.采用TUNEL法和蛋白质印迹法检测移植瘤组织的细胞凋亡指数(AI)及p53、c-Myc、Bax、Bcl-2、Survivin、Caspase-1、Fas蛋白的表达.应用不同浓度(0、50、100 μg/ml) MMI-166作用于人胰腺癌SW1990细胞24 h,蛋白质印迹法检测c-Myc、Survivin的表达.结果 MMI-166组移植瘤组织的AI为81.1±7.9,显著高于对照组的21.3±2.2 (P =0.000)；c-Myc、Survivin的表达量分别为7715±2229、4594±1240,显著低于对照组的16870±2446、15208±1903(P值均为0.000)；p53、Bax、Bcl-2、Caspase-1、Fas的表达与对照组比较无显著变化.50、100 μg/ml的MMI-166处理后,人胰腺癌SW1990细胞的c-Myc表达量显著下调(0.098±0.003、0.073±0.008比0.169±0.007,F=189.361,P＜0.05);Survivin 的表达量无明显变化.结论 MMI-166可能通过下调c-Myc的表达诱导人胰腺癌SW1990细胞凋亡.
目的 觀察MMI-166對人胰腺癌SW1990細胞及其移植瘤組織凋亡相關蛋白錶達的影響,探討其可能機製.方法 應用人胰腺癌細胞株SW1990建立裸鼠胰腺癌皮下移植瘤模型,按完全隨機法將荷瘤裸鼠分為對照組和MMI-166組,分彆給予口服生理鹽水和MMI-166(200 mg·kg-1·d-1),持續28 d.採用TUNEL法和蛋白質印跡法檢測移植瘤組織的細胞凋亡指數(AI)及p53、c-Myc、Bax、Bcl-2、Survivin、Caspase-1、Fas蛋白的錶達.應用不同濃度(0、50、100 μg/ml) MMI-166作用于人胰腺癌SW1990細胞24 h,蛋白質印跡法檢測c-Myc、Survivin的錶達.結果 MMI-166組移植瘤組織的AI為81.1±7.9,顯著高于對照組的21.3±2.2 (P =0.000)；c-Myc、Survivin的錶達量分彆為7715±2229、4594±1240,顯著低于對照組的16870±2446、15208±1903(P值均為0.000)；p53、Bax、Bcl-2、Caspase-1、Fas的錶達與對照組比較無顯著變化.50、100 μg/ml的MMI-166處理後,人胰腺癌SW1990細胞的c-Myc錶達量顯著下調(0.098±0.003、0.073±0.008比0.169±0.007,F=189.361,P＜0.05);Survivin 的錶達量無明顯變化.結論 MMI-166可能通過下調c-Myc的錶達誘導人胰腺癌SW1990細胞凋亡.
목적 관찰MMI-166대인이선암SW1990세포급기이식류조직조망상관단백표체적영향,탐토기가능궤제.방법 응용인이선암세포주SW1990건립라서이선암피하이식류모형,안완전수궤법장하류라서분위대조조화MMI-166조,분별급여구복생리염수화MMI-166(200 mg·kg-1·d-1),지속28 d.채용TUNEL법화단백질인적법검측이식류조직적세포조망지수(AI)급p53、c-Myc、Bax、Bcl-2、Survivin、Caspase-1、Fas단백적표체.응용불동농도(0、50、100 μg/ml) MMI-166작용우인이선암SW1990세포24 h,단백질인적법검측c-Myc、Survivin적표체.결과 MMI-166조이식류조직적AI위81.1±7.9,현저고우대조조적21.3±2.2 (P =0.000)；c-Myc、Survivin적표체량분별위7715±2229、4594±1240,현저저우대조조적16870±2446、15208±1903(P치균위0.000)；p53、Bax、Bcl-2、Caspase-1、Fas적표체여대조조비교무현저변화.50、100 μg/ml적MMI-166처리후,인이선암SW1990세포적c-Myc표체량현저하조(0.098±0.003、0.073±0.008비0.169±0.007,F=189.361,P＜0.05);Survivin 적표체량무명현변화.결론 MMI-166가능통과하조c-Myc적표체유도인이선암SW1990세포조망.
Objective To investigate the effects of MMI-166 on apoptosis and apoptosis-related protein expression of human pancreatic cancer SW1990 cells and its transplanted tumor,and explore possible mechanism.Methods The human pancreatic cancer xenograft model was constructed by using human pancreatic cancer SW1990 cells.Tumor-bearing nude mice were randomly divided into control and MMI-166 groups,and they were treated with normal saline or MMI-166 (200 mg · kg-1 · d-1) for 28 days.Apoptosis index (AI),p53,c-Myc,Bax,Bcl-2,Survivin,Caspase-1,Fas proteins were detected by deoxynucl-eotidyl transferase-mediated nick end labeling (TUNEL method) and Western blot.MMI-166 of different concentrations (0,50,100 μg/ml) were used to treat human pancreatic cancer SW1990 cell for 24 h.The c-Myc,Survivin proteins expressions were measured by Western blotting.Results Apoptosis index in MMI-166 group was 81.1 ±7.9,which was significantly higher than that in control group (21.3 ±2.2,P =0.000) ; the expressions of c-Myc,Survivin were 7715 ± 2229,4594 ± 1240,which were significantly higher than those in control group (16870 ± 2446,15208 ± 1903,P =0.000) ; the expressions of p53,Bax,Bcl-2,Caspase-1,Fas were not significantly different from those in control group.After 50,100 μg/ml MMI-166 treatment,the expression of c-Myc was significantly down-regulated (0.098 ± 0.003,0.073 ± 0.008 vs.0.169 ± 0.007,F =189.361,P ＜ 0.05) ; and the expression of Survivin was not significantly changed.Conclusions MMI-166 may induce cell apoptosis of SW1990 by down-regulating the expression of c-Myc.
