医学研究生学报
醫學研究生學報
의학연구생학보
JOURNAL OF MEDICAL POSTGRADUATE
2014年
10期
1023-1027
,共5页
孙兆瑞%杨志洲%林金锋%邵旦兵%刘红梅%徐敏%张炜%孙宝迪%任艺%邵斌霞%许宝华%唐文杰%聂时南
孫兆瑞%楊誌洲%林金鋒%邵旦兵%劉紅梅%徐敏%張煒%孫寶迪%任藝%邵斌霞%許寶華%唐文傑%聶時南
손조서%양지주%림금봉%소단병%류홍매%서민%장위%손보적%임예%소빈하%허보화%당문걸%섭시남
GES-1细胞%肠三叶因子%增殖%调控%PI3K/Akt信号通路
GES-1細胞%腸三葉因子%增殖%調控%PI3K/Akt信號通路
GES-1세포%장삼협인자%증식%조공%PI3K/Akt신호통로
GES-1 cells%Intestinal trefoil factor%Proliferation%Regulation%PI3K/Akt signaling pathway
目的：肠三叶因子（ intestinal trefoil factor ， ITF）对胃黏膜具有保护作用，但其机制尚不明确。文中探讨重组ITF对胃黏膜上皮细胞增殖能力的影响及其可能作用的分子机制。方法将体外培养的GES-1细胞分为3组，其中1组作为细胞增殖活力实验空白对照组，其他2组分别加入浓度为100和500 ng/mL的人重组ITF形成低浓度ITF组和高浓度ITF组。光镜下观察细胞形态，并采用CCK-8试剂盒检测GES-1细胞的增殖活力。体外培养的GES-1细胞株分别用100 ng/mL的ITF和浓度为15μmol/L的PI3 K/Akt 信号通路抑制剂LY294002进行处理，分为信号通路蛋白表达实验空白对照组、ITF组、LY294002组和ITF＋LY294002组，光镜下观察细胞形态。随后采用CCK-8试剂盒检测GES-1细胞处理后的增殖活力，采用Western blot检测PI3K/Akt信号通路中p-Akt和Akt蛋白的表达情况。结果与空白对照组相比， ITF刺激下GES-1细胞增殖活力明显增强，且ITF浓度越高、增殖活力越强。使用LY294002处理后，能够显著抑制ITF刺激的细胞增殖。 Western blot检测结果表明，ITF提高了p-Akt蛋白的表达水平，激活PI3K/Akt信号通路。结论 ITF促进GES-1细胞的增殖，推测其分子作用机制主要是通过激活PI3K/Akt信号通路促进细胞增殖。
目的：腸三葉因子（ intestinal trefoil factor ， ITF）對胃黏膜具有保護作用，但其機製尚不明確。文中探討重組ITF對胃黏膜上皮細胞增殖能力的影響及其可能作用的分子機製。方法將體外培養的GES-1細胞分為3組，其中1組作為細胞增殖活力實驗空白對照組，其他2組分彆加入濃度為100和500 ng/mL的人重組ITF形成低濃度ITF組和高濃度ITF組。光鏡下觀察細胞形態，併採用CCK-8試劑盒檢測GES-1細胞的增殖活力。體外培養的GES-1細胞株分彆用100 ng/mL的ITF和濃度為15μmol/L的PI3 K/Akt 信號通路抑製劑LY294002進行處理，分為信號通路蛋白錶達實驗空白對照組、ITF組、LY294002組和ITF＋LY294002組，光鏡下觀察細胞形態。隨後採用CCK-8試劑盒檢測GES-1細胞處理後的增殖活力，採用Western blot檢測PI3K/Akt信號通路中p-Akt和Akt蛋白的錶達情況。結果與空白對照組相比， ITF刺激下GES-1細胞增殖活力明顯增彊，且ITF濃度越高、增殖活力越彊。使用LY294002處理後，能夠顯著抑製ITF刺激的細胞增殖。 Western blot檢測結果錶明，ITF提高瞭p-Akt蛋白的錶達水平，激活PI3K/Akt信號通路。結論 ITF促進GES-1細胞的增殖，推測其分子作用機製主要是通過激活PI3K/Akt信號通路促進細胞增殖。
목적：장삼협인자（ intestinal trefoil factor ， ITF）대위점막구유보호작용，단기궤제상불명학。문중탐토중조ITF대위점막상피세포증식능력적영향급기가능작용적분자궤제。방법장체외배양적GES-1세포분위3조，기중1조작위세포증식활력실험공백대조조，기타2조분별가입농도위100화500 ng/mL적인중조ITF형성저농도ITF조화고농도ITF조。광경하관찰세포형태，병채용CCK-8시제합검측GES-1세포적증식활력。체외배양적GES-1세포주분별용100 ng/mL적ITF화농도위15μmol/L적PI3 K/Akt 신호통로억제제LY294002진행처리，분위신호통로단백표체실험공백대조조、ITF조、LY294002조화ITF＋LY294002조，광경하관찰세포형태。수후채용CCK-8시제합검측GES-1세포처리후적증식활력，채용Western blot검측PI3K/Akt신호통로중p-Akt화Akt단백적표체정황。결과여공백대조조상비， ITF자격하GES-1세포증식활력명현증강，차ITF농도월고、증식활력월강。사용LY294002처리후，능구현저억제ITF자격적세포증식。 Western blot검측결과표명，ITF제고료p-Akt단백적표체수평，격활PI3K/Akt신호통로。결론 ITF촉진GES-1세포적증식，추측기분자작용궤제주요시통과격활PI3K/Akt신호통로촉진세포증식。
Objective To explore the effects of intestinal trefoil factor ( ITF) on gastric mucosal epithelial cell proliferation and its possible molecular mechanism . Methods The cultured GES-1 cells were treated with ITF in the concentration of 100 ng/mL and 500 ng/mL in vitro, and then were observed using microscope for the morphological analysis .The Cell Counting Kit-8 ( CCK-8) was used to detect the proliferation activity of GES-1.The cultured GES-1 cells were treated with 100 ng/mL ITF and the specific inhibitor of PI3K/Akt signaling pathway LY294002 (15μmol/L) in vitro, and then were observed using microscope for the morphological analysis . The proliferation activity of treated GES-1cells was detected using CCK-8 and the expressions of p-Akt and Akt of PI3K/Akt signaling pathway were determined by Western blot . Results Compared with the control group , the proliferation activity of GES-1 cells in-creased after being treated with ITF and the higher concentration of ITF induced the higher proliferation activity .LY294002 inhibited the increased proliferation activity of GES-1induced by ITF.The data of Western blot indicated that ITF induced the expression of p -Akt and activated the P3IK/Akt signaling pathway to modulate the proliferation activity of GES -1 cells.However, LY294002 inhibited the PI3K/Akt signaling pathway and then decreased the proliferation activity of GES -1 cells. Conclusion ITF could promote the proliferation ac-tivity of GES-1 cells by activating PI3K/Akt signaling pathway .
