河南医学研究
河南醫學研究
하남의학연구
HENAN MEDICAL RESEARCH
2006年
1期
1-9
,共9页
步星耀%孔众%李作凌%张峰%张永福
步星耀%孔衆%李作凌%張峰%張永福
보성요%공음%리작릉%장봉%장영복
脑胶质瘤%尿激酶受体%治疗结果%血管生成%凋亡
腦膠質瘤%尿激酶受體%治療結果%血管生成%凋亡
뇌효질류%뇨격매수체%치료결과%혈관생성%조망
urokinase receptor%brain glioma%angiogenesis%adhesion%apoptosis%dhesion
目的:探讨尿激酶型纤溶酶原激活因子受体在人脑胶质瘤发生发展中的作用及靶向阻断对胶质瘤生长的影响.方法:采用人脑胶质瘤细胞U87MG建立高度重复性原位裸小鼠人脑胶质瘤模型,皮下应用鼠PEG-uPA 1-48(300μg)或人PEG-uPA 1-48(300μg)或者二者联合(各100μg)每周2次.结果:对照组9周内死亡,人PEG-uPA 1-48治疗组12周内死亡,20周后有20%鼠PEG-uPA 1-48治疗组和80%联合治疗组生存.组织学检测显示鼠PEG-uPA 1-48治疗组和联合治疗组肿瘤组织血管密度、细胞增殖指数显著降低,肿瘤细胞凋亡指数显著增加.结论:uPAR在胶质瘤的恶性演进中起重要作用,Peg-uPA能有效抑制脑胶质瘤生长,对脑胶质瘤辅助治疗有用.
目的:探討尿激酶型纖溶酶原激活因子受體在人腦膠質瘤髮生髮展中的作用及靶嚮阻斷對膠質瘤生長的影響.方法:採用人腦膠質瘤細胞U87MG建立高度重複性原位裸小鼠人腦膠質瘤模型,皮下應用鼠PEG-uPA 1-48(300μg)或人PEG-uPA 1-48(300μg)或者二者聯閤(各100μg)每週2次.結果:對照組9週內死亡,人PEG-uPA 1-48治療組12週內死亡,20週後有20%鼠PEG-uPA 1-48治療組和80%聯閤治療組生存.組織學檢測顯示鼠PEG-uPA 1-48治療組和聯閤治療組腫瘤組織血管密度、細胞增殖指數顯著降低,腫瘤細胞凋亡指數顯著增加.結論:uPAR在膠質瘤的噁性縯進中起重要作用,Peg-uPA能有效抑製腦膠質瘤生長,對腦膠質瘤輔助治療有用.
목적:탐토뇨격매형섬용매원격활인자수체재인뇌효질류발생발전중적작용급파향조단대효질류생장적영향.방법:채용인뇌효질류세포U87MG건립고도중복성원위라소서인뇌효질류모형,피하응용서PEG-uPA 1-48(300μg)혹인PEG-uPA 1-48(300μg)혹자이자연합(각100μg)매주2차.결과:대조조9주내사망,인PEG-uPA 1-48치료조12주내사망,20주후유20%서PEG-uPA 1-48치료조화80%연합치료조생존.조직학검측현시서PEG-uPA 1-48치료조화연합치료조종류조직혈관밀도、세포증식지수현저강저,종류세포조망지수현저증가.결론:uPAR재효질류적악성연진중기중요작용,Peg-uPA능유효억제뇌효질류생장,대뇌효질류보조치료유용.
Objective: To investigate the exact role of urokinase-type plasminogen activator receptor (uPAR) in the development of glioma and the inhibition of glioma growth by uPAR ligands. Methods: A highly reproducible or thotopic brain model has been established in nude mice using the human brain tumor cell line U87MG. Animals xenotransplanted with these tumor cells were treated twice a week subcutaneously with 300 μg/mouse of either mouse or human Peg-uPA 1-48 or a combination of 100 μg of each after the establishment of the tumors. Results: Control animals died within 9 weeks and human Peg-uPA treated animals within 12 weeks from progressive tumor growth. Twenty percent of the mice treated with mouse Peg-uPA and 80% of the mice receiving the combination of both peptides survived over 20 weeks. Histological examination demonstrated a decreased vascularity and tumor cell proliferation, a increased tumor cell apoptosis. Conclusion: uPAR plays a prodominant role in glioma progression. Peg-uPA can effectively inhibit brain glioma growth and might prove to be useful for adjuvant treatment of brain glioma.