山东医科大学学报
山東醫科大學學報
산동의과대학학보
ACTA ACADEMIAE MEDICINAE SHANDONG
2001年
2期
145-146
,共2页
燕东亮%刘丽%石缨%刘立忠%谢宝树
燕東亮%劉麗%石纓%劉立忠%謝寶樹
연동량%류려%석영%류립충%사보수
核转录因子-κB%肿瘤坏死因子%前列腺肿瘤
覈轉錄因子-κB%腫瘤壞死因子%前列腺腫瘤
핵전록인자-κB%종류배사인자%전렬선종류
探讨NF-κBI(NF-κB抑制剂)与融合基因PSP94-TNFαD11a联合注射抗前列腺癌的
作用。方法：制作PC-3细胞裸鼠动物模型。肌注PSP94与TNFαD11a融合基因的pcDNA-PSP94-TNFαD11a真核表达质粒DNA，并联合肌注NF-κBI，同时设pcDNA-PSP94、pcDNA-PSP94联用NF-κBI、pcDNA-PSP94-TNFαD11a、NF-κBI、空载体、生理盐水和环磷酰胺对照组。注射后第10天处死动物，称瘤重、计算押瘤率。结果：pcDNA-PSP94-TNFαD11a联合NF-κBI用药组抑瘤率(36％)高于pcDNA-PSP94-TNFαD11a组(20％)，前者瘤重〔(1.87±0.934)g〕明显低于后者〔(2.32±1.373)g〕。差异具有显著性(P<0.05)。结论：NF-κBI可提高TNF的抗前列腺癌作用。
探討NF-κBI(NF-κB抑製劑)與融閤基因PSP94-TNFαD11a聯閤註射抗前列腺癌的
作用。方法：製作PC-3細胞裸鼠動物模型。肌註PSP94與TNFαD11a融閤基因的pcDNA-PSP94-TNFαD11a真覈錶達質粒DNA，併聯閤肌註NF-κBI，同時設pcDNA-PSP94、pcDNA-PSP94聯用NF-κBI、pcDNA-PSP94-TNFαD11a、NF-κBI、空載體、生理鹽水和環燐酰胺對照組。註射後第10天處死動物，稱瘤重、計算押瘤率。結果：pcDNA-PSP94-TNFαD11a聯閤NF-κBI用藥組抑瘤率(36％)高于pcDNA-PSP94-TNFαD11a組(20％)，前者瘤重〔(1.87±0.934)g〕明顯低于後者〔(2.32±1.373)g〕。差異具有顯著性(P<0.05)。結論：NF-κBI可提高TNF的抗前列腺癌作用。
탐토NF-κBI(NF-κB억제제)여융합기인PSP94-TNFαD11a연합주사항전렬선암적
작용。방법：제작PC-3세포라서동물모형。기주PSP94여TNFαD11a융합기인적pcDNA-PSP94-TNFαD11a진핵표체질립DNA，병연합기주NF-κBI，동시설pcDNA-PSP94、pcDNA-PSP94련용NF-κBI、pcDNA-PSP94-TNFαD11a、NF-κBI、공재체、생리염수화배린선알대조조。주사후제10천처사동물，칭류중、계산압류솔。결과：pcDNA-PSP94-TNFαD11a연합NF-κBI용약조억류솔(36％)고우pcDNA-PSP94-TNFαD11a조(20％)，전자류중〔(1.87±0.934)g〕명현저우후자〔(2.32±1.373)g〕。차이구유현저성(P<0.05)。결론：NF-κBI가제고TNF적항전렬선암작용。
To analyse the effect of NF-κB on the cytotoxity of TNF to prostate cancer.Methods:pcDNA-PSP94-TNFαD11a plasmid was injected to the nude mice only once when the implanted PC-3 tumor grew to 4mm3, in combination with NF-κBI injection once daily for 10 days. The control groups were constructed. The animals were killed and tumors were weighted and tumor suppression rate was counted. Re
sults:Tumor suppression rates of the test group (36%) and the group that injected pcDNA-PSP94-TNFαD11a (20%) had significant difference (P<0.05). Conclusion: NF-κBI can increase the effects of TNF on prostate cancer significantly in vivo.
