【摘要】 目的 觀察晚期糖基化終產(chǎn)物（advanced glycosylation end prodrcts，AGE）對人結(jié)腸癌細(xì)胞株SW-480增殖的影響，并探討其可能機(jī)制?！》椒ā〔煌瑵舛華GE干預(yù)SW-480細(xì)胞，噻唑藍(lán)（MTT）法比較各組細(xì)胞活力，流式細(xì)胞術(shù)觀察AGE對SW-480細(xì)胞周期的影響，蛋白質(zhì)印跡法觀察AGE對SW-480細(xì)胞CyclinD1表達(dá)的影響，端粒重復(fù)序列擴(kuò)增法（telomeric repeat amplification protocol，TRAP）銀染法觀察AGE對SW-480細(xì)胞端粒酶活性的影響。MTT測細(xì)胞活力的檢測設(shè)置空白對照組、100 μg/mL小牛血清白蛋白（bovine serum albumin，BSA）組及50、100、500 μg/mL AGE組，其余檢測只設(shè)置100 μg/mL BSA組和100 μg/mL AGE組?！〗Y(jié)果 MTT結(jié)果示AGE促進(jìn)SW-480細(xì)胞的增殖，且呈濃度依賴性。100 μg/mL BSA組與100 μg/mL AGE組72 h后的細(xì)胞G0/G1期所占百分比分別為56.02%±0.58%、51.93%±1.01%，差異有統(tǒng)計學(xué)意義（Plt;0.05）。蛋白質(zhì)印跡法示100 μg/mL AGE組72 h后CyclinD1的表達(dá)較100 μg/mL BSA組增加，差異有統(tǒng)計學(xué)意義（Plt;0.05）。TRAP銀染法檢測示100 μg/mL AGE干預(yù)SW-480細(xì)胞72 h后可以增加端粒酶活性（Plt;0.05）?！〗Y(jié)論 AGE可促進(jìn)人結(jié)腸癌細(xì)胞SW-480生長，呈劑量依賴性。其作用機(jī)制可能與AGE上調(diào)CyclinD1的表達(dá)加速G1/S期轉(zhuǎn)換及增加端粒酶活性有關(guān)?！続bstract】 Objective To observe the effects of advanced glycosylation end products (AGE) on proliferation of SW-480 cells and study the possible mechanism. Methods Various concentrations of AGE were designed to have impact on SW-480 cells. Proliferation of SW-480 cells was assessed by thiazolyl blue tetrazolium bromide (MTT) assay; The impact of AGE on the cell cycle of SW-480 cells was analyzed by flow cytometry (FCM); the influence of AGE on expression of CyclinD1 was checked by Western blotting; and the impact of AGE on telomerase activity was examined by telomeric repeat amplification proctol (TRAP) sliver staining. For the MTT assay, blank control group, 100 μg/mL bovine serum albumin (BSA) group, 50, 100 and 500 μg/mL AGE groups were designed, while for other examinations, there were only 100 μg/mL BSA group and 100 μg/mL AGE group. Results MTT result showed that AGE increased the proliferation of SW-480 cells in a dose-dependent mode. The proportion of the cells at G0/G1 stage of the 100 μg/mL BSA group and the 100 μg/mL AGE experimental group were (56.02±0.58)% and (51.93±1.01)% respectively after 72 hours, with a significant difference (Plt;0.05); western blotting showed that the expression of CyclinD1 in the 100 μg/mL AGE group was significantly higher than that in the 100 μg/mL BSA group after 72 hours; TRAP silver staining demonstrated that telomerase activity increased significantly after treated with 100 μg/mL AGE for 72 hours. Conclusions AGE can promote the growth of SW-480 cells in a dose-dependent mode. Its mechanism is mainly by up-regulating the expression of CyclinD1 to shorten G0/G1 and increasing the telomerase activity significantly.