中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2015年
7期
548-552
,共5页
孙维建%胡丹红%李丕宏%卢明东%吴昊%周香%林海鸿%屠洋洋%俞耀军
孫維建%鬍丹紅%李丕宏%盧明東%吳昊%週香%林海鴻%屠洋洋%俞耀軍
손유건%호단홍%리비굉%로명동%오호%주향%림해홍%도양양%유요군
胃肿瘤%水通道蛋白质1%丝裂原活化蛋白激酶类
胃腫瘤%水通道蛋白質1%絲裂原活化蛋白激酶類
위종류%수통도단백질1%사렬원활화단백격매류
Stomach neoplasms%Aquaproin 1%Mitogen-activated protein kinases
目的 探讨曲古抑菌素A(TSA)通过P38丝裂原激活蛋白激酶信号通路调节胃癌细胞水通道蛋白1(aquaporin 1,AQP1)的表达.方法 用不同浓度的TSA处理胃癌SGC-7901细胞,MTT法检测细胞增殖情况,光镜和透射电镜下观察形态学改变,免疫组化及Western blot方法检测P38、磷酸化P38(p-P38)及AQP1的表达.实验分4组:对照组、TSA组、TSA+ SB203580(P38MAPK通路抑制剂)组、SB203580组.结果 (1)胃癌SGC-7901细胞的胞质及胞膜中均有棕褐色AQP1的阳性染色.不同药物作用后,各组AQP1表达定位未见变化.(2) TSA能够抑制细胞增殖,随着药物浓度的增加和作用时间的延长抑制率逐渐增加.(3)不同浓度TSA作用5h后,各组胃癌细胞中总P38表达相比差异均无统计学意义(均P ＞0.05),p-P38和AQP1表达水平比较差异均有统计学意义(均P＜0.05).TSA作用的最适宜浓度为100 nmol/L.(4)不同浓度SB203580作用5h后,胃癌细胞中总P38表达比较差异均无统计学意义(均P＞0.05);p-P38和AQP1表达水平比较差异均有统计学意义(均P＜ 0.05).SB203580作用的最适宜浓度为10 μmol/L.(5)用SB203580预处理胃癌细胞株2h后加入TSA 100 nmol/L作用组与不经过SB203580预处理而直接加用TSA作用各组的p-P38和AQP1相比差异有统计学意义(P＜0.01).结论 TSA通过P38丝裂原激活蛋白激酶信号通路对胃癌细胞AQP1的表达起调控作用.
目的 探討麯古抑菌素A(TSA)通過P38絲裂原激活蛋白激酶信號通路調節胃癌細胞水通道蛋白1(aquaporin 1,AQP1)的錶達.方法 用不同濃度的TSA處理胃癌SGC-7901細胞,MTT法檢測細胞增殖情況,光鏡和透射電鏡下觀察形態學改變,免疫組化及Western blot方法檢測P38、燐痠化P38(p-P38)及AQP1的錶達.實驗分4組:對照組、TSA組、TSA+ SB203580(P38MAPK通路抑製劑)組、SB203580組.結果 (1)胃癌SGC-7901細胞的胞質及胞膜中均有棕褐色AQP1的暘性染色.不同藥物作用後,各組AQP1錶達定位未見變化.(2) TSA能夠抑製細胞增殖,隨著藥物濃度的增加和作用時間的延長抑製率逐漸增加.(3)不同濃度TSA作用5h後,各組胃癌細胞中總P38錶達相比差異均無統計學意義(均P ＞0.05),p-P38和AQP1錶達水平比較差異均有統計學意義(均P＜0.05).TSA作用的最適宜濃度為100 nmol/L.(4)不同濃度SB203580作用5h後,胃癌細胞中總P38錶達比較差異均無統計學意義(均P＞0.05);p-P38和AQP1錶達水平比較差異均有統計學意義(均P＜ 0.05).SB203580作用的最適宜濃度為10 μmol/L.(5)用SB203580預處理胃癌細胞株2h後加入TSA 100 nmol/L作用組與不經過SB203580預處理而直接加用TSA作用各組的p-P38和AQP1相比差異有統計學意義(P＜0.01).結論 TSA通過P38絲裂原激活蛋白激酶信號通路對胃癌細胞AQP1的錶達起調控作用.
목적 탐토곡고억균소A(TSA)통과P38사렬원격활단백격매신호통로조절위암세포수통도단백1(aquaporin 1,AQP1)적표체.방법 용불동농도적TSA처리위암SGC-7901세포,MTT법검측세포증식정황,광경화투사전경하관찰형태학개변,면역조화급Western blot방법검측P38、린산화P38(p-P38)급AQP1적표체.실험분4조:대조조、TSA조、TSA+ SB203580(P38MAPK통로억제제)조、SB203580조.결과 (1)위암SGC-7901세포적포질급포막중균유종갈색AQP1적양성염색.불동약물작용후,각조AQP1표체정위미견변화.(2) TSA능구억제세포증식,수착약물농도적증가화작용시간적연장억제솔축점증가.(3)불동농도TSA작용5h후,각조위암세포중총P38표체상비차이균무통계학의의(균P ＞0.05),p-P38화AQP1표체수평비교차이균유통계학의의(균P＜0.05).TSA작용적최괄의농도위100 nmol/L.(4)불동농도SB203580작용5h후,위암세포중총P38표체비교차이균무통계학의의(균P＞0.05);p-P38화AQP1표체수평비교차이균유통계학의의(균P＜ 0.05).SB203580작용적최괄의농도위10 μmol/L.(5)용SB203580예처리위암세포주2h후가입TSA 100 nmol/L작용조여불경과SB203580예처리이직접가용TSA작용각조적p-P38화AQP1상비차이유통계학의의(P＜0.01).결론 TSA통과P38사렬원격활단백격매신호통로대위암세포AQP1적표체기조공작용.
Objective To investigate the effects of TSA on AQP1 in gastric cancer through P38MAPK signal pathway.Methods Gastric cancer SGC-7901 cells were treated with TSA,or SB203580 inhibitor of P38MAPK signal pathway.The proliferation was detected by MTT assay.The morphological changes were observed with light microscope and transmission electron microscope.The expression of P38MAPK and phosphorylated P38 was detected by Western-blot.SGC-7901 cells was randomly divided into control group,TSA group,TSA + SB203580 group,and SB203580 group.Results (1) Brown staining of AQP1 was detected in both cell membrane and cytoplasm in each group.(2) TSA inhibits SGC-7901 growth in a dose-dependent and time-dependent manner.(3) After 5 hour TSA treatment the P38 expression did not vary among groups (P ＞ 0.05),while p-P38 and AQP1 protein expression significantly changed (P ＜ 0.05).(4) After 5 hours SB203580 treatment P38 expression did not vary among groups (P ＞ 0.05),while p-P38 and AQP1 protein expression were significantly changed (P ＜ 0.05).(5) Pretreatment of SGC-7901 cells with SB203580 lowered the level of p-P38 and AQP1 compared with controls (P ＜ 0.01).Conclusions TSA regulates AQP1 protein expression in human gastric cancer cell lines,possibly by a mechanism related to P38MAPK signal pathway.
