中华肝胆外科杂志
中華肝膽外科雜誌
중화간담외과잡지
CHINESE JOURNAL OF HEPATOBILIARY SURGERY
2010年
6期
435-438
,共4页
石毅%孙跃明%白剑锋%陆文熊%傅赞%赵翰林%苗毅
石毅%孫躍明%白劍鋒%陸文熊%傅讚%趙翰林%苗毅
석의%손약명%백검봉%륙문웅%부찬%조한림%묘의
胰腺肿瘤%生长激素%胰岛素样生长因子Ⅰ%胰岛素样生长因子Ⅱ%胰岛素样生长因子结合蛋白3
胰腺腫瘤%生長激素%胰島素樣生長因子Ⅰ%胰島素樣生長因子Ⅱ%胰島素樣生長因子結閤蛋白3
이선종류%생장격소%이도소양생장인자Ⅰ%이도소양생장인자Ⅱ%이도소양생장인자결합단백3
Pancreatic neoplasms%Growth hormone%Insulin-like growth factor-Ⅰ%Insulin-like growth factor-Ⅱ%Insulin-like growth factor binding proteino-3
目的 观察生长激素(GH)对胰腺癌细胞增殖及对肿瘤宿主胰岛素样生长因子Ⅰ,Ⅱ(IGF-Ⅰ,Ⅱ)-胰岛素样生长因子结合蛋白3(IGFBP3)通路的影响,初步探讨体内外实验差异的原因.方法 体外应用GH(50 ng/ml)24 h,48 h,72 h后计数胰腺癌细胞SW-1990,PANC-1及P3;选用BALB/C雌性裸小鼠35只,以SW-1990成瘤,测量瘤体积,成瘤裸鼠随机分为注射GH的实验组(GH组)及对照组(NS组),荷瘤裸鼠在最后依次注射GH后第1小时、2小时、6小时及24小时处死动物,心室穿刺抽血,切除肝脏,酶联免疫吸附法(ELISA)检测血清IGF-Ⅰ,-Ⅱ水平(P<0.05),蛋白印记(Western Blot)方法观察肝脏IGFBP3的相对光密度(ROD)变化.结果 GH在体外可加速胰腺癌细胞增殖但在体内不促进肿瘤生长;GH上调荷瘤宿主血清IGF-Ⅰ、Ⅱ水平;与GH刺激前(NS)相比,肝脏IGFBP3表达在GH刺激后1 h、2 h、6 h有显著提高(P<0.05),24 h有所减弱.结论 GH对胰腺癌细胞的作用存在一定的体内外差异;GH在体内通过提高IGF-Ⅰ、Ⅱ水平发挥效应,GH不刺激在体肿瘤生长可能与IGFBP3上调有关.
目的 觀察生長激素(GH)對胰腺癌細胞增殖及對腫瘤宿主胰島素樣生長因子Ⅰ,Ⅱ(IGF-Ⅰ,Ⅱ)-胰島素樣生長因子結閤蛋白3(IGFBP3)通路的影響,初步探討體內外實驗差異的原因.方法 體外應用GH(50 ng/ml)24 h,48 h,72 h後計數胰腺癌細胞SW-1990,PANC-1及P3;選用BALB/C雌性裸小鼠35隻,以SW-1990成瘤,測量瘤體積,成瘤裸鼠隨機分為註射GH的實驗組(GH組)及對照組(NS組),荷瘤裸鼠在最後依次註射GH後第1小時、2小時、6小時及24小時處死動物,心室穿刺抽血,切除肝髒,酶聯免疫吸附法(ELISA)檢測血清IGF-Ⅰ,-Ⅱ水平(P<0.05),蛋白印記(Western Blot)方法觀察肝髒IGFBP3的相對光密度(ROD)變化.結果 GH在體外可加速胰腺癌細胞增殖但在體內不促進腫瘤生長;GH上調荷瘤宿主血清IGF-Ⅰ、Ⅱ水平;與GH刺激前(NS)相比,肝髒IGFBP3錶達在GH刺激後1 h、2 h、6 h有顯著提高(P<0.05),24 h有所減弱.結論 GH對胰腺癌細胞的作用存在一定的體內外差異;GH在體內通過提高IGF-Ⅰ、Ⅱ水平髮揮效應,GH不刺激在體腫瘤生長可能與IGFBP3上調有關.
목적 관찰생장격소(GH)대이선암세포증식급대종류숙주이도소양생장인자Ⅰ,Ⅱ(IGF-Ⅰ,Ⅱ)-이도소양생장인자결합단백3(IGFBP3)통로적영향,초보탐토체내외실험차이적원인.방법 체외응용GH(50 ng/ml)24 h,48 h,72 h후계수이선암세포SW-1990,PANC-1급P3;선용BALB/C자성라소서35지,이SW-1990성류,측량류체적,성류라서수궤분위주사GH적실험조(GH조)급대조조(NS조),하류라서재최후의차주사GH후제1소시、2소시、6소시급24소시처사동물,심실천자추혈,절제간장,매련면역흡부법(ELISA)검측혈청IGF-Ⅰ,-Ⅱ수평(P<0.05),단백인기(Western Blot)방법관찰간장IGFBP3적상대광밀도(ROD)변화.결과 GH재체외가가속이선암세포증식단재체내불촉진종류생장;GH상조하류숙주혈청IGF-Ⅰ、Ⅱ수평;여GH자격전(NS)상비,간장IGFBP3표체재GH자격후1 h、2 h、6 h유현저제고(P<0.05),24 h유소감약.결론 GH대이선암세포적작용존재일정적체내외차이;GH재체내통과제고IGF-Ⅰ、Ⅱ수평발휘효응,GH불자격재체종류생장가능여IGFBP3상조유관.
Objective To investigate the effect of GH on proliferation of pancreatic cancer cells and observe the features of IGF-IGFBP3 pathway in the host after GH administration. Methods Pancreatic cancer cells (SW-1990,PANC-1 and P3) during exponential growth stage were harvested and cultured in medium containing growth hormone (50 ng/ml). After 24, 48 and 72 hours, cells were counted using a Coulter Counter. Thirty-five Athymic nude Balb/c mice were inoculated with SW-1990cells. When tumors became palpable after inoculation, animals were randomized to receive GH points (1 h, 2 h, 6 h, 24 after the last injection), plasma samples were gathered for subsequent ELISA determination and liver was rapidly incised for immune blotting analysis. Results The results revealed that GH stimulated cell growth in vitro. GH elevated levels of IGF-Ⅰ , Ⅱ at the 1st , 2nd , 6th hour after the last injection. GH augmented the expression of IGFBP3 in the liver of the host in vivo (1 h, 2 h, 6 h, 24 h, respectively). Conclusion Such proteins as IGF- Ⅰ and Ⅱ might be associated with mechanism of last effect of GH on tumor host. The up-regulation of IGFBP3 by GH administration in the host may help to explain the phenomena that GH doesn't accelerate growth of pancreatic tumor in vivo.