新医学
新醫學
신의학
NEW CHINESE MEDICINE
2013年
12期
813-817
,共5页
胶质细胞源性神经营养因子%胰腺癌%神经侵袭%促分裂原活化蛋白激酶%磷脂酰肌醇激酶-3
膠質細胞源性神經營養因子%胰腺癌%神經侵襲%促分裂原活化蛋白激酶%燐脂酰肌醇激酶-3
효질세포원성신경영양인자%이선암%신경침습%촉분렬원활화단백격매%린지선기순격매-3
Glial cell derived neurotrophic factor%Pancreatic cancer%Neural invasion%Mitogen-activated protein kinase%Phosphatidyl Inositol 3-kinase
目的：观察胶质细胞源性神经营养因子（GDNF）在胰腺癌细胞侵袭中的作用及可能的机制。方法四甲基偶氮唑盐（MTT）法分别检测促分裂原活化蛋白激酶通道（MAPK）阻断剂PD98059和磷脂酰肌醇3激酶通道（PI3K）阻断剂LY294002在不同浓度、不同作用时间条件下对胰腺癌细胞MIA Paca-2存活率的影响，利用Trans-well装置在boyden小室的下室中分别加入不同的细胞因子（GDNF、GDNF抗体、PD98059、LY294002），通过计数各组跨膜细胞的数量并进行统计学分析，检测GDNF对胰腺癌细胞的趋化作用和PD98059、LY294002的阻断效果。结果 MTT实验中，培养基中分别加入不同浓度的PD98059或LY294002后，在不同作用时间下胰腺癌细胞形态未发生明显改变，各组的细胞存活率总体水平大都维持在90％～100％，且随药物作用时间或药物浓度变化均无明显规律性变化。Trans-well实验中，下室中加入GDNF后增加了Boyden小室跨膜细胞数量，加入阻断剂PD98059后跨膜细胞数量明显减少，差异有统计学意义（P＝0.014），加入阻断剂LY294002后跨膜细胞数量有减少趋势，差异无统计学意义（P＝0.221），同时加入两种阻断剂后跨膜细胞数量减少，差异有统计学意义（P＜0.01）。结论 GDNF可增强胰腺癌细胞MIA Paca-2的侵袭转移能力，发挥这一作用的途径可能与MAPK通道和PI3 K通道有关。
目的：觀察膠質細胞源性神經營養因子（GDNF）在胰腺癌細胞侵襲中的作用及可能的機製。方法四甲基偶氮唑鹽（MTT）法分彆檢測促分裂原活化蛋白激酶通道（MAPK）阻斷劑PD98059和燐脂酰肌醇3激酶通道（PI3K）阻斷劑LY294002在不同濃度、不同作用時間條件下對胰腺癌細胞MIA Paca-2存活率的影響，利用Trans-well裝置在boyden小室的下室中分彆加入不同的細胞因子（GDNF、GDNF抗體、PD98059、LY294002），通過計數各組跨膜細胞的數量併進行統計學分析，檢測GDNF對胰腺癌細胞的趨化作用和PD98059、LY294002的阻斷效果。結果 MTT實驗中，培養基中分彆加入不同濃度的PD98059或LY294002後，在不同作用時間下胰腺癌細胞形態未髮生明顯改變，各組的細胞存活率總體水平大都維持在90％～100％，且隨藥物作用時間或藥物濃度變化均無明顯規律性變化。Trans-well實驗中，下室中加入GDNF後增加瞭Boyden小室跨膜細胞數量，加入阻斷劑PD98059後跨膜細胞數量明顯減少，差異有統計學意義（P＝0.014），加入阻斷劑LY294002後跨膜細胞數量有減少趨勢，差異無統計學意義（P＝0.221），同時加入兩種阻斷劑後跨膜細胞數量減少，差異有統計學意義（P＜0.01）。結論 GDNF可增彊胰腺癌細胞MIA Paca-2的侵襲轉移能力，髮揮這一作用的途徑可能與MAPK通道和PI3 K通道有關。
목적：관찰효질세포원성신경영양인자（GDNF）재이선암세포침습중적작용급가능적궤제。방법사갑기우담서염（MTT）법분별검측촉분렬원활화단백격매통도（MAPK）조단제PD98059화린지선기순3격매통도（PI3K）조단제LY294002재불동농도、불동작용시간조건하대이선암세포MIA Paca-2존활솔적영향，이용Trans-well장치재boyden소실적하실중분별가입불동적세포인자（GDNF、GDNF항체、PD98059、LY294002），통과계수각조과막세포적수량병진행통계학분석，검측GDNF대이선암세포적추화작용화PD98059、LY294002적조단효과。결과 MTT실험중，배양기중분별가입불동농도적PD98059혹LY294002후，재불동작용시간하이선암세포형태미발생명현개변，각조적세포존활솔총체수평대도유지재90％～100％，차수약물작용시간혹약물농도변화균무명현규률성변화。Trans-well실험중，하실중가입GDNF후증가료Boyden소실과막세포수량，가입조단제PD98059후과막세포수량명현감소，차이유통계학의의（P＝0.014），가입조단제LY294002후과막세포수량유감소추세，차이무통계학의의（P＝0.221），동시가입량충조단제후과막세포수량감소，차이유통계학의의（P＜0.01）。결론 GDNF가증강이선암세포MIA Paca-2적침습전이능력，발휘저일작용적도경가능여MAPK통도화PI3 K통도유관。
Objective To observe the effect and the possible mechanism of glial cell derived neuro-trophic factor (GDNF)on invasive pancreatic carcinoma. Methods Methyl thiazolyl tetrazolium (MTT) as-say were used to detect the effect of PD98059-blocker of mitogen-activated protein kinase (MAPK)pathway and LY294002-blocker of phosphatidyl inositol 3-kinase (PI3K)pathway on the survival rate of pancreatic cancer cell MIA Paca-2 under different drug dosage and different reaction time. Different cytokines (GDNF、anti-GDNF antibody、PD98059、LY294002)were added in the lower chamber of the boyden chamber. Trans-membrane cell numbers of each group were analyzed statistically. Chemotaxis of GDNF on pancreatic cancer cell and the blocking effect of PD98059 and LY294002 by Trans-well device were also analysed.Results In the MTT assay,pancreatic cancer cell morphology did not change significantly when treated with different concen-trations of PD98059 and LY294002 in different reaction time. No significant difference was identified in the survival rate of each group. The overall survival rate maintained mostly from 90%to 1 00%,There was no sig-nificant change with different action time or drug concentration. In the Trans-well assay,when treated with GD-NF,the number of trans-membrane cells in boyden chamber increases while reduces when treated with PD98059,with significance (P=0.01 4). LY29400 also reduce the number,but without significant (P=0.221 ). The difference is obvious when added with both blockers simutaneously (P<0.01 ). Conclusion GDNF can enhance the ability of invasive and metastatic ability of MIA Paca-2. The mechanism may relate with MAPK path and PI3 K pathway.
