中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2011年
8期
697-701
,共5页
姜玉婷%费素娟%陈复兴%刘军权%陈玲%李昳%陶征中
薑玉婷%費素娟%陳複興%劉軍權%陳玲%李昳%陶徵中
강옥정%비소연%진복흥%류군권%진령%리질%도정중
白藜芦醇%结肠癌细胞%γδT细胞
白藜蘆醇%結腸癌細胞%γδT細胞
백려호순%결장암세포%γδT세포
Resveratrol%Colon cancer cells%γδT cells
目的 观察白藜芦醇作用前后γδT细胞对结肠癌SW-1116细胞杀伤活性的变化,并探讨其发生的机制。方法 异戊烯焦磷酸法体外扩增人外周血γδT细胞,不同浓度的白藜芦醇作用于γδT细胞和结肠癌SW-1116细胞,四甲基偶氮唑蓝(MTT)法检测白藜芦醇对γδT细胞及结肠癌细胞的生长的影响;流式细胞术(FCM)检测白藜芦醇作用前后γδT细胞穿孔素、颗粒酶B、CD107a的表达;乳酸脱氢酶( LDH)释放法检测白藜芦醇对γδT细胞杀伤结肠癌SW-1l16细胞活性的影响。Western blot检测药物作用前后γδT细胞细胞外信号调节激酶(ERK1/2)蛋白的活性的变化。结果 白藜芦醇在0.39 ~3.125μmol/L时对γδT细胞的生长具有促进作用,对结肠癌SW-1116细胞作用不明显;经白藜芦醇诱导后γδT细胞的穿孔素、颗粒酶B、CD107a的表达显著高于对照组(P<0.05);对结肠癌SW-1116细胞的杀伤活性也显著高于未诱导组(P<0.05);经浓度为0.1~10 μmol/L白藜芦醇作用的γδT细胞的p-ERK1/2表达较对照组增加(P<0.05)。结论 白藜芦醇能够促进γδT细胞的增殖,并增强其对结肠癌SW-1116细胞的杀伤能力,其机制可能与上调γδT细胞表面的穿孔素、颗粒酶B、CD107a的表达及活化细胞外信号调节激酶等有关。
目的 觀察白藜蘆醇作用前後γδT細胞對結腸癌SW-1116細胞殺傷活性的變化,併探討其髮生的機製。方法 異戊烯焦燐痠法體外擴增人外週血γδT細胞,不同濃度的白藜蘆醇作用于γδT細胞和結腸癌SW-1116細胞,四甲基偶氮唑藍(MTT)法檢測白藜蘆醇對γδT細胞及結腸癌細胞的生長的影響;流式細胞術(FCM)檢測白藜蘆醇作用前後γδT細胞穿孔素、顆粒酶B、CD107a的錶達;乳痠脫氫酶( LDH)釋放法檢測白藜蘆醇對γδT細胞殺傷結腸癌SW-1l16細胞活性的影響。Western blot檢測藥物作用前後γδT細胞細胞外信號調節激酶(ERK1/2)蛋白的活性的變化。結果 白藜蘆醇在0.39 ~3.125μmol/L時對γδT細胞的生長具有促進作用,對結腸癌SW-1116細胞作用不明顯;經白藜蘆醇誘導後γδT細胞的穿孔素、顆粒酶B、CD107a的錶達顯著高于對照組(P<0.05);對結腸癌SW-1116細胞的殺傷活性也顯著高于未誘導組(P<0.05);經濃度為0.1~10 μmol/L白藜蘆醇作用的γδT細胞的p-ERK1/2錶達較對照組增加(P<0.05)。結論 白藜蘆醇能夠促進γδT細胞的增殖,併增彊其對結腸癌SW-1116細胞的殺傷能力,其機製可能與上調γδT細胞錶麵的穿孔素、顆粒酶B、CD107a的錶達及活化細胞外信號調節激酶等有關。
목적 관찰백려호순작용전후γδT세포대결장암SW-1116세포살상활성적변화,병탐토기발생적궤제。방법 이무희초린산법체외확증인외주혈γδT세포,불동농도적백려호순작용우γδT세포화결장암SW-1116세포,사갑기우담서람(MTT)법검측백려호순대γδT세포급결장암세포적생장적영향;류식세포술(FCM)검측백려호순작용전후γδT세포천공소、과립매B、CD107a적표체;유산탈경매( LDH)석방법검측백려호순대γδT세포살상결장암SW-1l16세포활성적영향。Western blot검측약물작용전후γδT세포세포외신호조절격매(ERK1/2)단백적활성적변화。결과 백려호순재0.39 ~3.125μmol/L시대γδT세포적생장구유촉진작용,대결장암SW-1116세포작용불명현;경백려호순유도후γδT세포적천공소、과립매B、CD107a적표체현저고우대조조(P<0.05);대결장암SW-1116세포적살상활성야현저고우미유도조(P<0.05);경농도위0.1~10 μmol/L백려호순작용적γδT세포적p-ERK1/2표체교대조조증가(P<0.05)。결론 백려호순능구촉진γδT세포적증식,병증강기대결장암SW-1116세포적살상능력,기궤제가능여상조γδT세포표면적천공소、과립매B、CD107a적표체급활화세포외신호조절격매등유관。
Objective To explore the effect of γδT cells on colonic cancer cell lines SW-1116 treated by resveratrol. Methods Amplification γδT cells of human peripheral blood in vitro by using isopentenylpyrophosphate. Different density resveratrol induced γδT cells and colonic cancer cell SW-1 116, methyl thiazolyl tetrazolium(MTT) detectde the effect of growth and proliferation when expression veratrol action to γδT cells and colonic cancer cell lines SW-1116. Flow cytometer( FCM )detectde the expression of porforin, granzymeB and CD107a on γδT cells before it treated by resveratrol and after that. γδT cells against colonic cancer cell lines SW-1116 were detectde by lactate dehydrogenase(LDH) releasing assay before and after treated by resveratrol.Western blot analyzed the liveness of extracellular signal-regulated kinase1/2 of γδT cells before it treated by resveratrol and after that. Results γδTcells would be proliferation when the density of resveratrol in 0.39-3.125 μmol/L, while the effect on colonic cancer cell lines SW-1116 was not significance. There was significant difference of the expression of porforin, ranzymeB and CD107a on γδT cells before it treated by resveratrol and after that ( P<0.05 ). γδT cells against colonic cancer cell lines SW-1116 treated by resveratrol was enhanced compared with control group( P<0.05 ) . The p-ERK 1/2expression of γδT cells enhanced when the density of resveratrol treated to γδT cells in 0.1-10 μmol/L( P<0.05 ). Conclusion Resveratrol could promote γδT cells, proliferation and strengthen the cytotoxicity of γδT cells against colonic cancer cell SW-1116, the mechanism might concerned with activating p-ERK1/2 and enhancing the expression of porforin, granzymeB and CD107a on γδT cells.