疑难病杂志
疑難病雜誌
의난병잡지
JOURNAL OF DIFFICULT AND COMPLICATED CASES
2014年
4期
399-402
,共4页
付鑫鑫%田志华%郝钢华%刘占稳%刘金%邢军
付鑫鑫%田誌華%郝鋼華%劉佔穩%劉金%邢軍
부흠흠%전지화%학강화%류점은%류금%형군
辛二酰苯胺异羟肟酸%宫颈癌%裸鼠%Bcl-2%Bax
辛二酰苯胺異羥肟痠%宮頸癌%裸鼠%Bcl-2%Bax
신이선분알이간우산%궁경암%라서%Bcl-2%Bax
Suberoylanilide hydroxamic acid%Cervical cancer%Nude mice%Bcl-2%Bax
目的:观察辛二酰苯胺异羟肟酸( SAHA)对裸鼠人宫颈癌移植瘤生长的抑制作用,并对药物作用机制进行探讨。方法培养人宫颈癌SiHa细胞接种至20只裸鼠右下肢背侧根部皮下,15 d后将成瘤的18只裸鼠随机分3组:空白对照组、SAHA1组(25 mg/kg)、SAHA2组(50 mg/kg),每组6只。连续4 d腹腔注射药物,间歇7 d,再连续给药4 d,1次/d。观察各组裸鼠宫颈癌移植瘤的生长情况,计算抑瘤率。免疫组化分析及Western blot方法检测各组移植瘤中的Bax及Bcl-2蛋白的表达。结果空白对照组抑廇率为0,SAHA1组为22.44%, SAHA2组为35.52%,2组比较差异有统计学意义( P <0.05)。用药后,SAHA2组裸鼠体质量低于空白对照组及SAHA1组( P <0.05)。SAHA1组与SAHA2组肿瘤体积均小于空白对照组,且SAHA2组小于SAHA1组( P均<0.05)。与空白对照组相比, SAHA1组与SAHA2组裸鼠肿瘤质量低,且SAHA2组低于SAHA1组,差异均有统计学意义( P均<0.05);免疫组化及蛋白印迹法检测结果显示,与空白对照组比较,SAHA1组、SAHA2组Bax蛋白均明显升高,Bcl-2蛋白均明显降低( P均<0.05)。而SAHA2组较SAHA1组变化更明显,差异有统计学意义( P均<0.05)。结论 SAHA可以有效抑制人宫颈癌SiHa细胞裸鼠移植瘤的生长,Bax/Bcl-2相关的细胞凋亡是其抑癌机制之一。
目的:觀察辛二酰苯胺異羥肟痠( SAHA)對裸鼠人宮頸癌移植瘤生長的抑製作用,併對藥物作用機製進行探討。方法培養人宮頸癌SiHa細胞接種至20隻裸鼠右下肢揹側根部皮下,15 d後將成瘤的18隻裸鼠隨機分3組:空白對照組、SAHA1組(25 mg/kg)、SAHA2組(50 mg/kg),每組6隻。連續4 d腹腔註射藥物,間歇7 d,再連續給藥4 d,1次/d。觀察各組裸鼠宮頸癌移植瘤的生長情況,計算抑瘤率。免疫組化分析及Western blot方法檢測各組移植瘤中的Bax及Bcl-2蛋白的錶達。結果空白對照組抑廇率為0,SAHA1組為22.44%, SAHA2組為35.52%,2組比較差異有統計學意義( P <0.05)。用藥後,SAHA2組裸鼠體質量低于空白對照組及SAHA1組( P <0.05)。SAHA1組與SAHA2組腫瘤體積均小于空白對照組,且SAHA2組小于SAHA1組( P均<0.05)。與空白對照組相比, SAHA1組與SAHA2組裸鼠腫瘤質量低,且SAHA2組低于SAHA1組,差異均有統計學意義( P均<0.05);免疫組化及蛋白印跡法檢測結果顯示,與空白對照組比較,SAHA1組、SAHA2組Bax蛋白均明顯升高,Bcl-2蛋白均明顯降低( P均<0.05)。而SAHA2組較SAHA1組變化更明顯,差異有統計學意義( P均<0.05)。結論 SAHA可以有效抑製人宮頸癌SiHa細胞裸鼠移植瘤的生長,Bax/Bcl-2相關的細胞凋亡是其抑癌機製之一。
목적:관찰신이선분알이간우산( SAHA)대라서인궁경암이식류생장적억제작용,병대약물작용궤제진행탐토。방법배양인궁경암SiHa세포접충지20지라서우하지배측근부피하,15 d후장성류적18지라서수궤분3조:공백대조조、SAHA1조(25 mg/kg)、SAHA2조(50 mg/kg),매조6지。련속4 d복강주사약물,간헐7 d,재련속급약4 d,1차/d。관찰각조라서궁경암이식류적생장정황,계산억류솔。면역조화분석급Western blot방법검측각조이식류중적Bax급Bcl-2단백적표체。결과공백대조조억류솔위0,SAHA1조위22.44%, SAHA2조위35.52%,2조비교차이유통계학의의( P <0.05)。용약후,SAHA2조라서체질량저우공백대조조급SAHA1조( P <0.05)。SAHA1조여SAHA2조종류체적균소우공백대조조,차SAHA2조소우SAHA1조( P균<0.05)。여공백대조조상비, SAHA1조여SAHA2조라서종류질량저,차SAHA2조저우SAHA1조,차이균유통계학의의( P균<0.05);면역조화급단백인적법검측결과현시,여공백대조조비교,SAHA1조、SAHA2조Bax단백균명현승고,Bcl-2단백균명현강저( P균<0.05)。이SAHA2조교SAHA1조변화경명현,차이유통계학의의( P균<0.05)。결론 SAHA가이유효억제인궁경암SiHa세포라서이식류적생장,Bax/Bcl-2상관적세포조망시기억암궤제지일。
Objective To observe the tumor growth inhibition effect of SAHA to human cervical cancer transplanted in nude mice and to discuss the mechanism .Methods Cultured human cancer cell lines in nude mice inoculated to 20 dorsal roots of the right lower limb subcutaneous , 15 d after the tumor will become 18 mice were randomly divided into three groups with each included 6 mice:blank control group, SAHA1 group (25 mg/kg), SAHA2 group (50 mg/kg).Consecutive 4d in-traperitoneal injection of drugs , intermittent 7 d, and then continuously administered 4 d, 1 times/d.Observe the growth of cancer xenografts in nude mice in each group , the inhibition rate was calculated .Immunohistochemistry and Western blot a-nalysis was used to detect the expression of tumor in each group Bax and Bcl-2 protein.Results Tumor suppression in blank control group was 0, SAHA1 group was 22.44%, SAHA2 group was 35.52% , the two groups was statistically significant difference ( P <0.05).After treatment, SAHA2 group nude body mass were lower than the blank control group and SAHA 1 group ( P <0.05).After treatment, SAHA1 group SAHA2 tumor volume was less than the blank control group , and the SA-HA2 group was less than SAHA1 group( P <0.05).Compared with the blank control group , SAHA1 group and SAHA2 nude mice's tumors with low quality, and SAHA2 group lower than SAHA1 group, the differences were statistically significant (P <0.05);in immunohistochemistry test and protein blotting method , compared with blank control group , tumor tissue Bax protein in SAHA1 group and SAHA2 group were significantly increased , Bcl-2 protein were significantly lowered ( P <0.05).the changes in SAHA2 group were more obvious than SAHA1 group ( P <0.05).Conclusion SAHA can inhibit human cancer xenograft SiHa cell growth , Bax/Bcl-2 -related apoptosis is one of the tumor suppressor mechanism .