东南大学学报（医学版）
東南大學學報（醫學版）
동남대학학보（의학판）
JOURNAL OF SOUTHEAST UNIVERSITY(MEDICAL SCIENCE EDITION)
2013年
4期
399-403
,共5页
晚期糖基化终产物%人肝癌HepG2细胞%多药耐药
晚期糖基化終產物%人肝癌HepG2細胞%多藥耐藥
만기당기화종산물%인간암HepG2세포%다약내약
advanced glycation end products%human hepatocellular carcinoma HepG 2 cells%multidrug resistance
目的：探讨晚期糖基化终产物（ advanced glycation end products ，AGEs）对肝癌细胞耐药性的影响及其机制。方法：体外培养人肝癌细胞HepG2，以终浓度分别为100、200、400μg· ml-1的AGEs联合2000 nmol· L-1盐酸阿霉素（ adramycin ，ADM）处理细胞24 h，并设空白对照和ADM组进行比较。应用倒置显微镜观察不同浓度AGEs联合ADM孵育下HepG2形态学变化，流式细胞术（ flow cytometry，FCM）检测细胞周期的改变，应用细胞计数试剂盒（ cell counting kit-8，CCK-8）检测细胞株活性，蛋白质免疫印迹法（ Western blotting ）测定不同浓度AGEs作用下，HepG2细胞多药耐药基因（ multidrug resistance-1，MDR1）蛋白表达情况。结果：在2000 nmol · L-1 ADM作用下，HepG2细胞生长停滞或死亡，而AGEs能促进细胞生长，抑制其死亡。细胞周期和细胞活性实验表明，与ADM组相比，随着AGEs浓度增加，G1期细胞百分率显著下降，S期及G2期细胞增加，细胞活性有上升趋势。 Western blotting检测表明AGEs能增加MDR1的蛋白表达。结论：AGEs能通过促进MDR1基因的表达，降低肿瘤细胞对化疗药物的敏感性。
目的：探討晚期糖基化終產物（ advanced glycation end products ，AGEs）對肝癌細胞耐藥性的影響及其機製。方法：體外培養人肝癌細胞HepG2，以終濃度分彆為100、200、400μg· ml-1的AGEs聯閤2000 nmol· L-1鹽痠阿黴素（ adramycin ，ADM）處理細胞24 h，併設空白對照和ADM組進行比較。應用倒置顯微鏡觀察不同濃度AGEs聯閤ADM孵育下HepG2形態學變化，流式細胞術（ flow cytometry，FCM）檢測細胞週期的改變，應用細胞計數試劑盒（ cell counting kit-8，CCK-8）檢測細胞株活性，蛋白質免疫印跡法（ Western blotting ）測定不同濃度AGEs作用下，HepG2細胞多藥耐藥基因（ multidrug resistance-1，MDR1）蛋白錶達情況。結果：在2000 nmol · L-1 ADM作用下，HepG2細胞生長停滯或死亡，而AGEs能促進細胞生長，抑製其死亡。細胞週期和細胞活性實驗錶明，與ADM組相比，隨著AGEs濃度增加，G1期細胞百分率顯著下降，S期及G2期細胞增加，細胞活性有上升趨勢。 Western blotting檢測錶明AGEs能增加MDR1的蛋白錶達。結論：AGEs能通過促進MDR1基因的錶達，降低腫瘤細胞對化療藥物的敏感性。
목적：탐토만기당기화종산물（ advanced glycation end products ，AGEs）대간암세포내약성적영향급기궤제。방법：체외배양인간암세포HepG2，이종농도분별위100、200、400μg· ml-1적AGEs연합2000 nmol· L-1염산아매소（ adramycin ，ADM）처리세포24 h，병설공백대조화ADM조진행비교。응용도치현미경관찰불동농도AGEs연합ADM부육하HepG2형태학변화，류식세포술（ flow cytometry，FCM）검측세포주기적개변，응용세포계수시제합（ cell counting kit-8，CCK-8）검측세포주활성，단백질면역인적법（ Western blotting ）측정불동농도AGEs작용하，HepG2세포다약내약기인（ multidrug resistance-1，MDR1）단백표체정황。결과：재2000 nmol · L-1 ADM작용하，HepG2세포생장정체혹사망，이AGEs능촉진세포생장，억제기사망。세포주기화세포활성실험표명，여ADM조상비，수착AGEs농도증가，G1기세포백분솔현저하강，S기급G2기세포증가，세포활성유상승추세。 Western blotting검측표명AGEs능증가MDR1적단백표체。결론：AGEs능통과촉진MDR1기인적표체，강저종류세포대화료약물적민감성。
Objective:To investigated the effects of advanced glycation end products (AGEs) on the multidrug resistance of HepG2 cells and its mechanism .Methods: Human hepatocellular carcinoma HepG 2 cells were cultured and exposed to AGEs at the concentration of 100,200 and 400μg· ml-1 combined with 2 000 nmol· L-1 adramycin( ADM) for 24 hours in vitro, normal control group and ADM group were established for comparison . Inverted microscope was used to observe the change of cell morphous .The flow cytometry ( FCM ) was used to investigate cell cycle and cell counting kit-8 ( CCK-8) assay was used to assess the cell activity .Western blotting was used to study protein expression of MDR 1.Results: In cell culture medium with 2 000 nmol · L-1 ADM, HepG2 showed arrest of growth and death , and AGEs could promote HepG 2 cell growth and prevent cell death . FCM and CCK-8 experimental results showed that the percentage of cells in G 1 phase declined significantly , S phase and G 2 phase increased , cell activity was significantly higher than ADM group , the phenomena were more obvious when AGEs concentration increasing .Western blotting experimental results showed that AGEs could increase protein expression of MDR1.Conclusion: AGEs could promote MDR of tumor cells to chemotherapy by increasing MDR1 gene expression .
