中国医科大学学报
中國醫科大學學報
중국의과대학학보
JOURNAL OF CHINA MEDICAL UNIVERSITY
2009年
10期
737-740
,共4页
HA14-1%Lewis肺癌%环磷酰胺%增敏
HA14-1%Lewis肺癌%環燐酰胺%增敏
HA14-1%Lewis폐암%배린선알%증민
HA14-1%Lewis lung carcinoma%cyclophamide%sensitization
目的 观察HA14-1对环磷酰胺(CTX)治疗Lewis肺癌小鼠的化疗增效作用,探讨其可能的作用机制.方法 建立Lewis肺癌小鼠肿瘤模型,将40只C57BL/6小鼠随机分为4组:生理盐水组、CTX组、HA14-1组和CTX+HA14-1组,给药7 d.于肿瘤接种22 d处死小鼠,描绘各组肿瘤体积增长曲线、计算抑瘤率,免疫组织化学方法测定治疗前后Lewis肺癌细胞Bcl-2、Bax和Caspase-9蛋白的表达情况.结果 HA14-1组与生理盐水组比较无明显抑制肿瘤体积的作用,CTX组、HA14-1组和CTX+HA14-1组的肿瘤体积较生理盐水组增长慢.HA14-1组的抑瘤率与生理盐水组比较无明显增加(P>0.05);CTX+HA14-1组及CTX组与生理盐水组比较,CTX+HA14-1组与CTX组比较,抑瘤率均明显增加(P<0.05).CTX组、HA14-1组和CTX+HA14-1组Bcl-2蛋白表达均减少,且CTX+HA14-1组较CTX组Bcl-2蛋白明显减少(P<0.05).CTX组、HA14-1组和CTX+HA14-1组Bax、Caspase-9蛋白表达增加,与生理盐水组比较差异有统计学意义(P<0.05);CTX+HA14-1组比CTX组Bax、Caspase-9蛋白表达明显增加(P<0.05).结论 HA14-1可以增加CTX的化疗作用,其作用机制可能是通过抑制Bcl-2蛋白的表达,增加Bax、Caspase-9蛋白表达,从而促使肿瘤细胞凋亡.
目的 觀察HA14-1對環燐酰胺(CTX)治療Lewis肺癌小鼠的化療增效作用,探討其可能的作用機製.方法 建立Lewis肺癌小鼠腫瘤模型,將40隻C57BL/6小鼠隨機分為4組:生理鹽水組、CTX組、HA14-1組和CTX+HA14-1組,給藥7 d.于腫瘤接種22 d處死小鼠,描繪各組腫瘤體積增長麯線、計算抑瘤率,免疫組織化學方法測定治療前後Lewis肺癌細胞Bcl-2、Bax和Caspase-9蛋白的錶達情況.結果 HA14-1組與生理鹽水組比較無明顯抑製腫瘤體積的作用,CTX組、HA14-1組和CTX+HA14-1組的腫瘤體積較生理鹽水組增長慢.HA14-1組的抑瘤率與生理鹽水組比較無明顯增加(P>0.05);CTX+HA14-1組及CTX組與生理鹽水組比較,CTX+HA14-1組與CTX組比較,抑瘤率均明顯增加(P<0.05).CTX組、HA14-1組和CTX+HA14-1組Bcl-2蛋白錶達均減少,且CTX+HA14-1組較CTX組Bcl-2蛋白明顯減少(P<0.05).CTX組、HA14-1組和CTX+HA14-1組Bax、Caspase-9蛋白錶達增加,與生理鹽水組比較差異有統計學意義(P<0.05);CTX+HA14-1組比CTX組Bax、Caspase-9蛋白錶達明顯增加(P<0.05).結論 HA14-1可以增加CTX的化療作用,其作用機製可能是通過抑製Bcl-2蛋白的錶達,增加Bax、Caspase-9蛋白錶達,從而促使腫瘤細胞凋亡.
목적 관찰HA14-1대배린선알(CTX)치료Lewis폐암소서적화료증효작용,탐토기가능적작용궤제.방법 건립Lewis폐암소서종류모형,장40지C57BL/6소서수궤분위4조:생리염수조、CTX조、HA14-1조화CTX+HA14-1조,급약7 d.우종류접충22 d처사소서,묘회각조종류체적증장곡선、계산억류솔,면역조직화학방법측정치료전후Lewis폐암세포Bcl-2、Bax화Caspase-9단백적표체정황.결과 HA14-1조여생리염수조비교무명현억제종류체적적작용,CTX조、HA14-1조화CTX+HA14-1조적종류체적교생리염수조증장만.HA14-1조적억류솔여생리염수조비교무명현증가(P>0.05);CTX+HA14-1조급CTX조여생리염수조비교,CTX+HA14-1조여CTX조비교,억류솔균명현증가(P<0.05).CTX조、HA14-1조화CTX+HA14-1조Bcl-2단백표체균감소,차CTX+HA14-1조교CTX조Bcl-2단백명현감소(P<0.05).CTX조、HA14-1조화CTX+HA14-1조Bax、Caspase-9단백표체증가,여생리염수조비교차이유통계학의의(P<0.05);CTX+HA14-1조비CTX조Bax、Caspase-9단백표체명현증가(P<0.05).결론 HA14-1가이증가CTX적화료작용,기작용궤제가능시통과억제Bcl-2단백적표체,증가Bax、Caspase-9단백표체,종이촉사종류세포조망.
Objective To observe HA14-1 sensitizes Lewis lung carcinoma in mice to cyclophosphamide (CTX) and to explore its possible mechanism. Methods Forty Lewis lung carcinoma model mice were randomly divided into 4 groups:normal saline group,CTX group, HA14-1 group,CTX+HA14-1 group. After the treatment of 7 days,all of the mice were killed on the 22nd day of tumor inoculation. The tumor volume growth curve of each group was described;tumor inhibition rate was caculatued;Bcl-2,Bax,Caspase-9 protein expression levels before and after the treatment were determined by immunohistnehemistry. Results Compared to the normal saline group,HA14-1 group had no significant effect on inhibiting tumor volume,and the tumor volume in HA14-1 group increased less slowly than that of CTX group, HA14-1 group and CTX+HA14-1 group. Compared to the normal saline group, the tumor inhibition rate of HA14-1 group had no significant increase (P> 0.05),while that of CTX group and CTX + HA14-1 group increased significantly (P< 0.05);compared to the CTX group,the tumor inhibition rate of CTX + HA14-1 group increased significantly (P < 0.05). Bcl-2 protein expression levels in CTX group,HA14-1 group and CTX+HA14-1 group were lower than that in the normal saline groups compared to CTX group,Bcl-2 protein expression of CTX + HA14-1 group reduced significantly. Compared to the normal saline group,the expression levels of Bax and Caspase-9 protein in CTX group, HA14-1 group and CTX+HA14-1 group increased significantly (P< 0.05);compared to CTX group,CTX + HA14-1 group increased more significantly (P < 0.05). Conclusion HA14-1 might enhance the efficiency of CTX chemotherapy via inhibiting the expression of Bcl-2, increasing the expression of Bax and caspase-9 and promoting tumor cell apoptosis.
