中国肿瘤生物治疗杂志
中國腫瘤生物治療雜誌
중국종류생물치료잡지
CHINESE JOURNAL OF CANCER BIOTHERAPY
2009年
6期
609-613
,共5页
蔡海东%谯娱%袁雪宇%杨越华%袁世栋%孙明%吕中伟
蔡海東%譙娛%袁雪宇%楊越華%袁世棟%孫明%呂中偉
채해동%초오%원설우%양월화%원세동%손명%려중위
聚乙烯亚胺-精氨酸-甘氨酸-天冬氨酸(PEI-RGD)%整合素α_v亚基%ASODN%肝肿瘤%侵袭
聚乙烯亞胺-精氨痠-甘氨痠-天鼕氨痠(PEI-RGD)%整閤素α_v亞基%ASODN%肝腫瘤%侵襲
취을희아알-정안산-감안산-천동안산(PEI-RGD)%정합소α_v아기%ASODN%간종류%침습
polyethyleneimine-Arg-Gly-Asp (PEI-RGD)%integrin α_v%antisense oligodeoxynueleotide (ASODN)%hepatocellular carcinoma%invasion
目的:探讨以PEI-RGD(polyethyleneimine-Arg-Gly-Asp)为转染载体的~(125)I-(α_v)ASODN投递在体外对HepG2肝癌细胞侵袭力的影响.方法:~(125)I标记整合素α_v亚基的ASODN,以聚乙烯亚胺衍生物PEI-RGD为载体制备PEI-RGD/~(125)I-(α_v)ASODN复合物,通过受体介导方式转染进入HepG2细胞,利用Boyden小室侵袭模型检测复合物对HepG2细胞侵袭力的影响.结果:(1)~(125)I-(α_v)ASODN的标记率为(73.78±4.09)%,放化纯度为(96.68±1.38)%.37℃放置48 h后的放化纯度仍>90%,表明其稳定性良好;(2)HepG2细胞对PEI-RGD/~(125)I-(α_v)ASODN的摄取于4μl/2 μg时达到峰值[(12.77±0.85)%],之后明显降低,故选择2μl/1μg作为PEI-RGD/~(125)I-(α_v)ASODN对HepG2细胞的作用剂量;(3)相对于其他实验组和对照组,PEI-RGD/~(125)I-(α_v)ASODN组显著降低了HepG2细胞的侵袭能力(P<0.01).结论:以PEI-RGD为载体投递~(125)I-(α_v)ASODN能有效抑制HepG2细胞的侵袭力.
目的:探討以PEI-RGD(polyethyleneimine-Arg-Gly-Asp)為轉染載體的~(125)I-(α_v)ASODN投遞在體外對HepG2肝癌細胞侵襲力的影響.方法:~(125)I標記整閤素α_v亞基的ASODN,以聚乙烯亞胺衍生物PEI-RGD為載體製備PEI-RGD/~(125)I-(α_v)ASODN複閤物,通過受體介導方式轉染進入HepG2細胞,利用Boyden小室侵襲模型檢測複閤物對HepG2細胞侵襲力的影響.結果:(1)~(125)I-(α_v)ASODN的標記率為(73.78±4.09)%,放化純度為(96.68±1.38)%.37℃放置48 h後的放化純度仍>90%,錶明其穩定性良好;(2)HepG2細胞對PEI-RGD/~(125)I-(α_v)ASODN的攝取于4μl/2 μg時達到峰值[(12.77±0.85)%],之後明顯降低,故選擇2μl/1μg作為PEI-RGD/~(125)I-(α_v)ASODN對HepG2細胞的作用劑量;(3)相對于其他實驗組和對照組,PEI-RGD/~(125)I-(α_v)ASODN組顯著降低瞭HepG2細胞的侵襲能力(P<0.01).結論:以PEI-RGD為載體投遞~(125)I-(α_v)ASODN能有效抑製HepG2細胞的侵襲力.
목적:탐토이PEI-RGD(polyethyleneimine-Arg-Gly-Asp)위전염재체적~(125)I-(α_v)ASODN투체재체외대HepG2간암세포침습력적영향.방법:~(125)I표기정합소α_v아기적ASODN,이취을희아알연생물PEI-RGD위재체제비PEI-RGD/~(125)I-(α_v)ASODN복합물,통과수체개도방식전염진입HepG2세포,이용Boyden소실침습모형검측복합물대HepG2세포침습력적영향.결과:(1)~(125)I-(α_v)ASODN적표기솔위(73.78±4.09)%,방화순도위(96.68±1.38)%.37℃방치48 h후적방화순도잉>90%,표명기은정성량호;(2)HepG2세포대PEI-RGD/~(125)I-(α_v)ASODN적섭취우4μl/2 μg시체도봉치[(12.77±0.85)%],지후명현강저,고선택2μl/1μg작위PEI-RGD/~(125)I-(α_v)ASODN대HepG2세포적작용제량;(3)상대우기타실험조화대조조,PEI-RGD/~(125)I-(α_v)ASODN조현저강저료HepG2세포적침습능력(P<0.01).결론:이PEI-RGD위재체투체~(125)I-(α_v)ASODN능유효억제HepG2세포적침습력.
Objective:To study the effects of ~(125)I-(α_v)ASODN on the in vitro invasive ability of heptocellular carcino-ma cell line(HepG2) through PEI-RGD-mediated receptor process. Methods: Intergrin α_v-specific antisense oligonucle-otide was labeled with ~(125)I, and PEI-RGD/~(125)I-(α_v)ASODN complex was prepared by combining ~(125)I-(α_v)ASODN with polyethyleneimine derivative PEI-RGD. PEI-RGD/~(125)I-(α_v)ASODN complex was transferred into HepG2 cells through the receptor-mediated process. The effect of PEI-RGD/~(125)I-(α_v)ASODN complex on the invasive ability of HepG2 cells was examined by Boyden chamber invasive assay. Results: (1) The labeling yield and radiochemical purity of ~(125)I-(α_v) ASODN were(73.78±4.09)% and(96.68±1.38)%, respectively, and the labeled compound had a good stability in vitro after 48 h at 37℃; (2) The ability of HepG2 cells to uptake PEI-RGD/~(125)I-(α_v)ASODN reached its peek ([12.77±0.85] % ) when PEI-RGD/~(125)I-(α_v)ASODN was at 4 μl/2 μg ([12.77±0.85] %), and then gredually decreased thereafter. So the dosage of PEI-RGD/~(125)I-(α_v)ASODN for the following experiment was chosen as 2 μl/1 μg; (3) The invasive capacity of HepG2 cells was significantly reduced in PEI-RGD/~(125)I-(α_v)ASODN group compared with those in other experiment and control groups (P <0.01 ). Conclusion: ~(125)I-(α_v)ASODN mediated by PEI-RGD can effectively inhibit the invasive capacity of HepG2 cells.