中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2014年
4期
635-639
,共5页
李力%金震东%蔡敏%王斌%程烽涛
李力%金震東%蔡敏%王斌%程烽濤
리력%금진동%채민%왕빈%정봉도
卡托普利%胃肿瘤%裸小鼠
卡託普利%胃腫瘤%裸小鼠
잡탁보리%위종류%라소서
Captopril%Stomach neoplasms%Nude mice
目的:观察血管紧张素转换酶抑制剂卡托普利对胃癌发生与发展的调控作用,探索其应用于胃癌临床治疗的可行性。方法:制备AGS裸鼠移植瘤模型,随机分为3组:阳性对照(5-氟尿嘧啶,5-Fu)组、对照(生理盐水)组和实验(卡托普利)组。各组分别腹腔注射或灌胃后,观察肿瘤生长情况,组织取样,采用实时荧光定量PCR和免疫组化法检测Ki-67、STAT3、Bax和Bcl-2表达情况,TUNEL+DAPI染色法检测细胞凋亡。 Western blotting检测STAT3及p-STAT3表达。结果:造模成功后,各组小鼠均出现差异不明显的肿瘤结块。14 d后,各组差异明显加大。对照组裸鼠肿瘤块生长最快,卡托普利组次之,阳性对照组最慢。实时荧光定量PCR与免疫组化检测结果显示,卡托普利组Bax较对照组表达升高,而STAT3、Ki-67以及Bcl-2的表达则降低(P<0.05),卡托普利组上述因子表达趋势与5-Fu组表达趋势相一致,但2组间差异显著( P<0.05);凋亡结果显示,相较于对照组,其它2组细胞凋亡率明显升高( P<0.05);Western blotting结果也显示,5-Fu组及卡托普利组的p-STAT3与STAT3蛋白表达水平较对照组明显降低(P<0.05)。结论:血管紧张素转换酶抑制剂卡托普利对AGS裸鼠胃癌有较为明显的治疗效果,推测其可能具有较为可行的应用性。其分子机制可能是通过对STAT3转录活化因子以及Bax、Bcl-2、Ki-67等的调控,促使肿瘤细胞凋亡或抑制其生长。
目的:觀察血管緊張素轉換酶抑製劑卡託普利對胃癌髮生與髮展的調控作用,探索其應用于胃癌臨床治療的可行性。方法:製備AGS裸鼠移植瘤模型,隨機分為3組:暘性對照(5-氟尿嘧啶,5-Fu)組、對照(生理鹽水)組和實驗(卡託普利)組。各組分彆腹腔註射或灌胃後,觀察腫瘤生長情況,組織取樣,採用實時熒光定量PCR和免疫組化法檢測Ki-67、STAT3、Bax和Bcl-2錶達情況,TUNEL+DAPI染色法檢測細胞凋亡。 Western blotting檢測STAT3及p-STAT3錶達。結果:造模成功後,各組小鼠均齣現差異不明顯的腫瘤結塊。14 d後,各組差異明顯加大。對照組裸鼠腫瘤塊生長最快,卡託普利組次之,暘性對照組最慢。實時熒光定量PCR與免疫組化檢測結果顯示,卡託普利組Bax較對照組錶達升高,而STAT3、Ki-67以及Bcl-2的錶達則降低(P<0.05),卡託普利組上述因子錶達趨勢與5-Fu組錶達趨勢相一緻,但2組間差異顯著( P<0.05);凋亡結果顯示,相較于對照組,其它2組細胞凋亡率明顯升高( P<0.05);Western blotting結果也顯示,5-Fu組及卡託普利組的p-STAT3與STAT3蛋白錶達水平較對照組明顯降低(P<0.05)。結論:血管緊張素轉換酶抑製劑卡託普利對AGS裸鼠胃癌有較為明顯的治療效果,推測其可能具有較為可行的應用性。其分子機製可能是通過對STAT3轉錄活化因子以及Bax、Bcl-2、Ki-67等的調控,促使腫瘤細胞凋亡或抑製其生長。
목적:관찰혈관긴장소전환매억제제잡탁보리대위암발생여발전적조공작용,탐색기응용우위암림상치료적가행성。방법:제비AGS라서이식류모형,수궤분위3조:양성대조(5-불뇨밀정,5-Fu)조、대조(생리염수)조화실험(잡탁보리)조。각조분별복강주사혹관위후,관찰종류생장정황,조직취양,채용실시형광정량PCR화면역조화법검측Ki-67、STAT3、Bax화Bcl-2표체정황,TUNEL+DAPI염색법검측세포조망。 Western blotting검측STAT3급p-STAT3표체。결과:조모성공후,각조소서균출현차이불명현적종류결괴。14 d후,각조차이명현가대。대조조라서종류괴생장최쾌,잡탁보리조차지,양성대조조최만。실시형광정량PCR여면역조화검측결과현시,잡탁보리조Bax교대조조표체승고,이STAT3、Ki-67이급Bcl-2적표체칙강저(P<0.05),잡탁보리조상술인자표체추세여5-Fu조표체추세상일치,단2조간차이현저( P<0.05);조망결과현시,상교우대조조,기타2조세포조망솔명현승고( P<0.05);Western blotting결과야현시,5-Fu조급잡탁보리조적p-STAT3여STAT3단백표체수평교대조조명현강저(P<0.05)。결론:혈관긴장소전환매억제제잡탁보리대AGS라서위암유교위명현적치료효과,추측기가능구유교위가행적응용성。기분자궤제가능시통과대STAT3전록활화인자이급Bax、Bcl-2、Ki-67등적조공,촉사종류세포조망혹억제기생장。
AIM:To observe the effect of captopril on the genesis and development of gastric cancer , and to explore its clinical treatment feasibility for gastric cancer .METHODS:The human gastric cancer cell line AGS was used to establish a tumor model in nude mice , and the model mice were randomly divided into 3 groups: positive control ( 5-fluorouracil) group, normal control (saline) group and experimental (captopril) group.After intraperitoneal injection or intragastric administration of the drugs , the tumor growth curve was determined , and the tumor tissues were also sampled to detect the expression of Ki-67, STAT3, Bax and Bcl-2 by real-time quantitative PCR and immunohistochemistry .The apop-tosis was detected by TUNEL +DAPI staining .RESULTS: The tumor growth curve showed that the tumor model in the nude mice was successfully established .The tumor volumes among groups showed significantly different after 14 d growth. The increase in the tumor volume in normal control group was significantly faster than that in the other two groups , and that in positive control group was the slowest .The expression of Bax in captopril group increased , and the expression of STAT3, Ki-67 and Bcl-2 was reduced as compared with normal control group and positive control group .Compared with normal con-trol group, the apoptotic rate increased significantly , and the protein expression of p-STAT3 and STAT3 decreased obviously in positive control group and captopril group .CONCLUSION:With better feasibility , angiotensin-converting enzyme in-hibitor captopril has a significant effect on treating gastric cancer in the AGS nude mouse model by regulating the expression of STAT3, Bax, Bcl-2 and Ki-67 to accelerate the apoptosis of cancer cells , thus inhibiting tumor growth .