中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2011年
6期
407-409
,共3页
周国雄%朱陈%丁晓凌%张海峰%张弘%曹维%强晖%徐正府
週國雄%硃陳%丁曉凌%張海峰%張弘%曹維%彊暉%徐正府
주국웅%주진%정효릉%장해봉%장홍%조유%강휘%서정부
胰腺肿瘤%MK886%Celecoxib%5-脂氧合酶%环氧化酶-2
胰腺腫瘤%MK886%Celecoxib%5-脂氧閤酶%環氧化酶-2
이선종류%MK886%Celecoxib%5-지양합매%배양화매-2
Pancreatic neoplasms%MK886%Celecoxib%5-Lipoxygenase%Cyclooxygenase
目的 观察5-脂氧合酶拮抗剂MK886、环氧化酶2拮抗剂Celeeoxib干预SW1990细胞后对细胞增殖及血管内皮生长因子(VEGF)mRNA表达的影响.方法 应用不同浓度的MK886、Celecoxib 以及两者联合处理SW1990细胞,采用胆囊收缩素(CCK-8)法检测细胞的增殖,RT-PCR法检测细胞白三烯B4受体1(BLT1) mRNA、前列腺素2(PGE2) mRNA、VEGF mRNA的表达.结果 10μmol/LMK886或20 mmol/L Celecoxib处理24h后,SW1990细胞的增殖受到明显抑制(1.80±0.06比1.65±0.10;2.04 ±0.03比1.86 ±0.02,P＜0.05),且随药物浓度的增加,细胞的增殖抑制更明显.两拮抗剂联合干预12h后,SW1990细胞的增殖即受到非常明显的抑制(1.72±0.05比1.52±0.05,P＜0.01).Celecoxib处理细胞48 h后,细胞BLT1、VEGF mRNA表达与对照组比较无明显变化,但PGE2 mRNA的表达明显减少(37.50比71.50,P＜0.05)；MK886或MK886+ Celecoxib联合处理细胞后,细胞BLT1、VEGF mRNA表达明显减少(40.30、22.75比126.50,P＜0.05),而PGE2 mRNA的表达与对照组比较无明显变化.结论 花生四烯酸的两条代谢途径均与胰腺癌的发生及增殖有密切关系,同时抑制两条途径可显著抑制胰腺癌细胞的增殖.
目的 觀察5-脂氧閤酶拮抗劑MK886、環氧化酶2拮抗劑Celeeoxib榦預SW1990細胞後對細胞增殖及血管內皮生長因子(VEGF)mRNA錶達的影響.方法 應用不同濃度的MK886、Celecoxib 以及兩者聯閤處理SW1990細胞,採用膽囊收縮素(CCK-8)法檢測細胞的增殖,RT-PCR法檢測細胞白三烯B4受體1(BLT1) mRNA、前列腺素2(PGE2) mRNA、VEGF mRNA的錶達.結果 10μmol/LMK886或20 mmol/L Celecoxib處理24h後,SW1990細胞的增殖受到明顯抑製(1.80±0.06比1.65±0.10;2.04 ±0.03比1.86 ±0.02,P＜0.05),且隨藥物濃度的增加,細胞的增殖抑製更明顯.兩拮抗劑聯閤榦預12h後,SW1990細胞的增殖即受到非常明顯的抑製(1.72±0.05比1.52±0.05,P＜0.01).Celecoxib處理細胞48 h後,細胞BLT1、VEGF mRNA錶達與對照組比較無明顯變化,但PGE2 mRNA的錶達明顯減少(37.50比71.50,P＜0.05)；MK886或MK886+ Celecoxib聯閤處理細胞後,細胞BLT1、VEGF mRNA錶達明顯減少(40.30、22.75比126.50,P＜0.05),而PGE2 mRNA的錶達與對照組比較無明顯變化.結論 花生四烯痠的兩條代謝途徑均與胰腺癌的髮生及增殖有密切關繫,同時抑製兩條途徑可顯著抑製胰腺癌細胞的增殖.
목적 관찰5-지양합매길항제MK886、배양화매2길항제Celeeoxib간예SW1990세포후대세포증식급혈관내피생장인자(VEGF)mRNA표체적영향.방법 응용불동농도적MK886、Celecoxib 이급량자연합처리SW1990세포,채용담낭수축소(CCK-8)법검측세포적증식,RT-PCR법검측세포백삼희B4수체1(BLT1) mRNA、전렬선소2(PGE2) mRNA、VEGF mRNA적표체.결과 10μmol/LMK886혹20 mmol/L Celecoxib처리24h후,SW1990세포적증식수도명현억제(1.80±0.06비1.65±0.10;2.04 ±0.03비1.86 ±0.02,P＜0.05),차수약물농도적증가,세포적증식억제경명현.량길항제연합간예12h후,SW1990세포적증식즉수도비상명현적억제(1.72±0.05비1.52±0.05,P＜0.01).Celecoxib처리세포48 h후,세포BLT1、VEGF mRNA표체여대조조비교무명현변화,단PGE2 mRNA적표체명현감소(37.50비71.50,P＜0.05)；MK886혹MK886+ Celecoxib연합처리세포후,세포BLT1、VEGF mRNA표체명현감소(40.30、22.75비126.50,P＜0.05),이PGE2 mRNA적표체여대조조비교무명현변화.결론 화생사희산적량조대사도경균여이선암적발생급증식유밀절관계,동시억제량조도경가현저억제이선암세포적증식.
Objective To investigate the effects of two inhibitors of arachidonic acid metabolic pathway (5-cyclooxygenase blockade MK886 and COX 2 blockade celecoxib) on growth and VEGF mRNA expression of human pancreatic cancer cell SW1990.Methods Pancreatic cancer cells SW1990 were cultured with different concentrations of MK886,celecoxib,MK886 and celecoxib,then the cell proliferation was detected by using CCK-8,BLT1 mRNA,PGE2 mRNA and VEGF mRNA expressions were determined by RTPCR.Results After 10 μmol/L MK886 or 20 mmol/L celecoxib treatment for 24 h,the growth of SW1990 was greatly suppressed ( 1.80 ±0.06 vs 1.65 ±0.10,2.04 ±0.03 vs 1.86 ±0.02,P ＜0.01 ),and the growth suppression of SW1990 cells was increased accompanying the raised concentration of MK886 or celecoxib.After both MK886 and celecoxib treatment for 12 h,the growth of SW 1990 cells was much obviously suppressed (1.72 ±0.05 vs 1.52 ±0.05,P ＜0.01 ).After celecoxib treatment for 48 h,the BLT1 mRNA,PGE2 mRNA and VEGFmRNA expressions were not significantly changed,but the expressions of PGE2 mRNA were significantly decreased ( P ＜ 0.05 ).After MK886 or MK886 + celecoxib treatment,the expressions of BLT1 mRNA,VEGF mRNA were significantly decreased ( P ＜ 0.05 ),but the expressions of PGE2 mRNA were not significantly changed when compared to control group.Conclusions Two metabolic pathways of arachidonic acid have a close relation with occurrence and proliferation of pancreatic cancer,when both of the pathways were blocked,the proliferation of the pancreatic cancer cell was suppressed obviously.
