中华胃肠外科杂志
中華胃腸外科雜誌
중화위장외과잡지
CHINESE JOURNAL OF GASTROINTESTINAL SURGERY
2008年
4期
376-378
,共3页
曾庆黎%楚朝辉%周凯%罗小江
曾慶黎%楚朝輝%週凱%囉小江
증경려%초조휘%주개%라소강
结肠肿瘤%肿瘤转移%血管生成%血管生成抑制剂%微血管密度
結腸腫瘤%腫瘤轉移%血管生成%血管生成抑製劑%微血管密度
결장종류%종류전이%혈관생성%혈관생성억제제%미혈관밀도
Colorectal neoplasm%Neoplasm metastasis%Angiogenesis%Angiogenesis inhibitor%Micrevessel density
目的 探讨血管生成抑制剂Endostatin和SU6668联合氟尿嘧啶(5-FU)对结肠癌生长和转移的抑制作用,并探讨其作用机制.方法 建立人结肠癌裸鼠原位种植转移模型.将60只荷瘤鼠随机分为5组,每组12只.种植12 d后分别自腹腔内注射生理盐水(对照组)、Endostatin(E组)、SU6668(S组)、Endostatin加SU6668(E加S组)、Endostatin加SU6668加5-FU(E加S加F组),1次/d,共4周.种植后第6周末处死动物,测量原位肿瘤瘤重、抑瘤率和肿瘤微血管密度(MVD),观察肿瘤肝腹膜和区域淋巴结转移及腹水出现情况.结果 对照组、E组、S组、E加S组、E加S加F组抑瘤率分别为0、64.9%、63.5%、76.4%和88.2%;MVD分别为(18.10±5.65)、(2.75±0.75)、(3.17±0.58)、(0.94±0.42)和(0.36±0.45);腹膜转移率分别为90%、16.7%、25%、0和0;区域淋巴结转移率分别为90%、0、0、0和0.E组、S组、E加S组、E加S加F组与对照组相比,结肠癌生长和转移受到明显抑制(P<0.05);尤以E加S加F组明显(P<0.01).结论 Endostatin和SU6668联合5-F1U具有协同作用,能更有效地抑制结肠癌的生长和转移.
目的 探討血管生成抑製劑Endostatin和SU6668聯閤氟尿嘧啶(5-FU)對結腸癌生長和轉移的抑製作用,併探討其作用機製.方法 建立人結腸癌裸鼠原位種植轉移模型.將60隻荷瘤鼠隨機分為5組,每組12隻.種植12 d後分彆自腹腔內註射生理鹽水(對照組)、Endostatin(E組)、SU6668(S組)、Endostatin加SU6668(E加S組)、Endostatin加SU6668加5-FU(E加S加F組),1次/d,共4週.種植後第6週末處死動物,測量原位腫瘤瘤重、抑瘤率和腫瘤微血管密度(MVD),觀察腫瘤肝腹膜和區域淋巴結轉移及腹水齣現情況.結果 對照組、E組、S組、E加S組、E加S加F組抑瘤率分彆為0、64.9%、63.5%、76.4%和88.2%;MVD分彆為(18.10±5.65)、(2.75±0.75)、(3.17±0.58)、(0.94±0.42)和(0.36±0.45);腹膜轉移率分彆為90%、16.7%、25%、0和0;區域淋巴結轉移率分彆為90%、0、0、0和0.E組、S組、E加S組、E加S加F組與對照組相比,結腸癌生長和轉移受到明顯抑製(P<0.05);尤以E加S加F組明顯(P<0.01).結論 Endostatin和SU6668聯閤5-F1U具有協同作用,能更有效地抑製結腸癌的生長和轉移.
목적 탐토혈관생성억제제Endostatin화SU6668연합불뇨밀정(5-FU)대결장암생장화전이적억제작용,병탐토기작용궤제.방법 건립인결장암라서원위충식전이모형.장60지하류서수궤분위5조,매조12지.충식12 d후분별자복강내주사생리염수(대조조)、Endostatin(E조)、SU6668(S조)、Endostatin가SU6668(E가S조)、Endostatin가SU6668가5-FU(E가S가F조),1차/d,공4주.충식후제6주말처사동물,측량원위종류류중、억류솔화종류미혈관밀도(MVD),관찰종류간복막화구역림파결전이급복수출현정황.결과 대조조、E조、S조、E가S조、E가S가F조억류솔분별위0、64.9%、63.5%、76.4%화88.2%;MVD분별위(18.10±5.65)、(2.75±0.75)、(3.17±0.58)、(0.94±0.42)화(0.36±0.45);복막전이솔분별위90%、16.7%、25%、0화0;구역림파결전이솔분별위90%、0、0、0화0.E조、S조、E가S조、E가S가F조여대조조상비,결장암생장화전이수도명현억제(P<0.05);우이E가S가F조명현(P<0.01).결론 Endostatin화SU6668연합5-F1U구유협동작용,능경유효지억제결장암적생장화전이.
Objective To investigate the effect of Endostatin and SU6668 combined with 5-FU on the growth and metastasis of human colon cancer in vivo and its mechanism. Methods Metastatic model of human colon cancer was established by orthotopic implantation of human tumor tissue into colon wall of nude mice. Twelve days later, mice were randomly divided into saline water control, Ensostatin, SU6668, Ensostatin plus SU6668, and Endostatin plus SU6668 and 5-FU groups, intraperitoneal injected respectively every day for four weeks. Six weeks after implication, the tumor weight, inhibition rates, intratumoral microvessel density (MVD) and metastasis were evaluated after the mice were sacrificed. Results Compared with the control, tumor growth was significantly inhibited in mice treated respectively with Ensostatin, SU6668, Ensostatin plus SU6668 and Endostatin plus SU6668 and 5-FU with an inhibition rate of 0, 64.9%, 63.5%, 76.4% and 88.2% respectively, and MVD decreased significantly in treated groups [(18.10±5.65) vs (2.75±0.75), (3.17±0.58), (0.94±0.42) and (0.36±0.45)]. The incidences of peritoneal and region lymph node metastases were significantly inhibited in Ensostatin, SU6668, Ensostatin plus SU6668 and Endostatin plus SU6668 and 5-FU (90% vs 16.7%, 25%, 0 and 0; 90% vs 0, 0, 0 and 0). The growth and metastasis of human colon cancer implanted in nude mice were significantly inhibited in Ensostatin, SU6668, Easostatin plus SU6668, and Endostatin plus SU6668 and 5-FU, and the effect of Endostatin plus SU6668 and 5-FU was the most obviously. Conclusion Endostatin plus SU6668 and 5-FU has strong inhibitory effect both on tumor growth and metastasis of human colon cancer.
