中华核医学杂志
中華覈醫學雜誌
중화핵의학잡지
CHINESE JOURNAL OF NUCLEAR MEDICINE
2009年
2期
92-95
,共4页
崔永刚%张春丽%王荣福%闫平%于明明%刘红洁%付占立%郭凤琴%赵媛%刘萌%康磊%丁义
崔永剛%張春麗%王榮福%閆平%于明明%劉紅潔%付佔立%郭鳳琴%趙媛%劉萌%康磊%丁義
최영강%장춘려%왕영복%염평%우명명%류홍길%부점립%곽봉금%조원%류맹%강뢰%정의
黑色素瘤%肿瘤细胞%培养的%肽类%环%碘放射性同位素%小鼠
黑色素瘤%腫瘤細胞%培養的%肽類%環%碘放射性同位素%小鼠
흑색소류%종류세포%배양적%태류%배%전방사성동위소%소서
Melanoma%Tumor cells,cultured%Peptides,cyclic%Iodine radioisotopes%Mice
目的 用131I标记环精氨酸-甘氨酸-天冬氨酸(cRGD)肽-探讨131I-cRGD对荷黑色素瘤小鼠模型瘤体生长的双重抑制作用.方法 应用氯胺T法对cRGD进行131I标记.建立荷黑色素瘤B16株小鼠模型,将20只荷瘤小鼠按完全随机化法分为4组,每组5只.即实验(131I-cRGD)组、cRGD对照组、131I-甘氨酸-甘氨酸-甘氨酸(cGGG)对照组和空白对照(PBS)组.分别经尾静脉注射相应药物,观察各组倚瘤小鼠肿瘤体积和质量的变化,利用单因素方差分析比较各组之间的差异.结果 131I-cRGD的标记率和放化纯分别达到(89.14±4.57)%及(99.14±0.72)%.治疗第2l天时.各组与PBS组肿瘤体积相比.抑瘤率分别为64.92%(131I-cRGD组)、37.70%(cRGD组)及24.78%(131I-cGGG组);治疗第28天时,处死各组小鼠,其瘤质量(含治疗第2l～28天自然死亡的4只小鼠)分别为131I-cRGD组(6.48±5.19)g、cRGD组(10.81±6.25)g、131I-cGGG组(14.21±5.91)g、PBS组(18.88±7.59)g(F=3.479,P<0.05),131I-cRGD组与PBS组之间差异有统计学意义(t=3.12,P<0.05).各组与PBS组肿瘤质量相比,抑瘤率分别为65.72%(131I-cRGD组)、42.76%(cRGD组)及24.77%(131I-cGGG组).治疗第28天时,各组小鼠净体质量(净体质量=小鼠体质量一瘤质量,含治疗第2l～28天死亡的4只小鼠)分别为(29.12±8.66)g(131I-cRGD组)、(25.89±6.49)g(cRGD组)、(24.29±2.97)g(131I-cGGG组)、(20.92±5.95)g(PBS组).差异尤统计学意义(F=1.444,P>0.05).结论 131I-cRGD能抑制荷黑色素瘤小鼠肿瘤的生长,对黑色素瘤治疗具有潜在的价值.
目的 用131I標記環精氨痠-甘氨痠-天鼕氨痠(cRGD)肽-探討131I-cRGD對荷黑色素瘤小鼠模型瘤體生長的雙重抑製作用.方法 應用氯胺T法對cRGD進行131I標記.建立荷黑色素瘤B16株小鼠模型,將20隻荷瘤小鼠按完全隨機化法分為4組,每組5隻.即實驗(131I-cRGD)組、cRGD對照組、131I-甘氨痠-甘氨痠-甘氨痠(cGGG)對照組和空白對照(PBS)組.分彆經尾靜脈註射相應藥物,觀察各組倚瘤小鼠腫瘤體積和質量的變化,利用單因素方差分析比較各組之間的差異.結果 131I-cRGD的標記率和放化純分彆達到(89.14±4.57)%及(99.14±0.72)%.治療第2l天時.各組與PBS組腫瘤體積相比.抑瘤率分彆為64.92%(131I-cRGD組)、37.70%(cRGD組)及24.78%(131I-cGGG組);治療第28天時,處死各組小鼠,其瘤質量(含治療第2l～28天自然死亡的4隻小鼠)分彆為131I-cRGD組(6.48±5.19)g、cRGD組(10.81±6.25)g、131I-cGGG組(14.21±5.91)g、PBS組(18.88±7.59)g(F=3.479,P<0.05),131I-cRGD組與PBS組之間差異有統計學意義(t=3.12,P<0.05).各組與PBS組腫瘤質量相比,抑瘤率分彆為65.72%(131I-cRGD組)、42.76%(cRGD組)及24.77%(131I-cGGG組).治療第28天時,各組小鼠淨體質量(淨體質量=小鼠體質量一瘤質量,含治療第2l～28天死亡的4隻小鼠)分彆為(29.12±8.66)g(131I-cRGD組)、(25.89±6.49)g(cRGD組)、(24.29±2.97)g(131I-cGGG組)、(20.92±5.95)g(PBS組).差異尤統計學意義(F=1.444,P>0.05).結論 131I-cRGD能抑製荷黑色素瘤小鼠腫瘤的生長,對黑色素瘤治療具有潛在的價值.
목적 용131I표기배정안산-감안산-천동안산(cRGD)태-탐토131I-cRGD대하흑색소류소서모형류체생장적쌍중억제작용.방법 응용록알T법대cRGD진행131I표기.건립하흑색소류B16주소서모형,장20지하류소서안완전수궤화법분위4조,매조5지.즉실험(131I-cRGD)조、cRGD대조조、131I-감안산-감안산-감안산(cGGG)대조조화공백대조(PBS)조.분별경미정맥주사상응약물,관찰각조의류소서종류체적화질량적변화,이용단인소방차분석비교각조지간적차이.결과 131I-cRGD적표기솔화방화순분별체도(89.14±4.57)%급(99.14±0.72)%.치료제2l천시.각조여PBS조종류체적상비.억류솔분별위64.92%(131I-cRGD조)、37.70%(cRGD조)급24.78%(131I-cGGG조);치료제28천시,처사각조소서,기류질량(함치료제2l～28천자연사망적4지소서)분별위131I-cRGD조(6.48±5.19)g、cRGD조(10.81±6.25)g、131I-cGGG조(14.21±5.91)g、PBS조(18.88±7.59)g(F=3.479,P<0.05),131I-cRGD조여PBS조지간차이유통계학의의(t=3.12,P<0.05).각조여PBS조종류질량상비,억류솔분별위65.72%(131I-cRGD조)、42.76%(cRGD조)급24.77%(131I-cGGG조).치료제28천시,각조소서정체질량(정체질량=소서체질량일류질량,함치료제2l～28천사망적4지소서)분별위(29.12±8.66)g(131I-cRGD조)、(25.89±6.49)g(cRGD조)、(24.29±2.97)g(131I-cGGG조)、(20.92±5.95)g(PBS조).차이우통계학의의(F=1.444,P>0.05).결론 131I-cRGD능억제하흑색소류소서종류적생장,대흑색소류치료구유잠재적개치.
Objective Ectogenic Arg-Gly-Asp(RGD)peptide can bind to integrin α2 β3 receptor on the cell membrane of tumor cells and neovasculature endothelial cells to prevent tumor growth and metas-tasis but was less potent than cRGD.The aim of this study wag to further understand the inhibitory effect of cRGD labeled with 131I in melanoma bearing mice.Methods cRGD peptide was labeled with 131I by Ch-T method under the optimum labeling conditions.Twenty mice were randomly (complete randomization) di-vided into four groups.five for each group.There were experimental group(131I-cRGD),cRGD control group.131l-Gly-Gly-Gly(cGGG)control group and phosphate buffered saline(PBS)control group.All mice were injected through tail vein.Tumor volume, weight and net weight (net weight =weight-the weight of the tumor)were measured for all and compared by one-way ANOVA.Results The labeling effi-ciency and the radiochemical purity of 131I-cRGD peptide were(89.14±4.57)%and(99.14±O.72)%respectively.Compared with the PBS group at 21st day, the tumor inhibitory rates were 64.92%for 131I-cRGD group.37.70% for cRGD group,and 24.78%for 131I-cGGG group respectively.When sacrificed at 28th day,the weight was(6.48±5.19)g for 131I-cRGD group,(10.81±6.25)g for cRGD group, (14.21±5.91)g for 131I-cGGG group,and(18.88±7.59)g for PBS group(F=3.479,P<0.05).Significant difference was observed between 131I-cRGD group and PBS group(t=3.12,P<0.05).Corn- pared with the PBS group at the end of treatment,the tumor inhibitory rates were 65.72%for 131I-cRGD group,42.76% for cRGD group,and 24.77%for 131I-cGGG group respectively and with net weight of (29.12±8.66)g for 131I-cRGD group,(25.89±6.49)g for cRGD group.(24.29 ±2.97)g for".I-cGGG group,and(20.92±5.95)g for PBS group(F=1.444,P>0.05).Conclusion 131I-cRGD could effectively inhibit tumor growth in melanoma bearing mice and might be of potential in treating melano-ma in, the future.
