摘要
目的糖尿病患者结肠癌的发病率显著高于非糖尿病人群,晚期糖基化终产物(advanced glycation end products,AGEs)在糖尿病患者体内生成明显增多。文中观察AGEs对人结肠癌细胞SW-480增殖的影响及其机制。方法体外培养人结肠癌细胞SW-480,以终浓度分别为100μg/ml、200μg/ml、500μg/ml的AGE-BSA处理细胞24h,并设正常对照组和BSA对照组进行比较。采用四甲基偶氮唑盐(MTT)法检测SW-480细胞活力,利用流式细胞术检测细胞周期的改变,实时荧光定量PCR测定晚期糖基化终产物受体(receptor for advanced glycation end products,RAGE)mRNA、细胞周期素D1(cyclin D1)mRNA的表达。结果①MTT结果示100μg/ml、200μg/ml、500μg/mlAGE-BSA作用SW-480细胞24 h后可以显著促进细胞增殖(P<0.05),并呈浓度依赖性。②流式细胞术结果示200μg/mlAGE-BSA干预组24 h后可以减少SW-480细胞G1期百分率,同时增加S期百分率,与正常对照组比较具有统计学差异(P<0.05)。③实时荧光定量PCR结果示与正常对照组相比,200μg/mlAGE-BSA干预后可以上调RAGEmRNA和cyclin D1 mRNA的表达(P<0.05)。结论 AGEs能促进SW-480细胞的增殖,其机制可能与上调RAGEmRNA和cyclin D1 mRNA的表达,加速细胞G1期向S期转换相关。
Objective The incidence of colon cancer is significantly higher in diabetic patients than in non-diabetic population,and advanced glycation end products（AGEs） increase in diabetes mellitus.This study investigated the effect of AGEs on the proliferation of SW-480 cells and its mechanism.Methods Human colon carcinoma SW-480 cells were cultured and exposed to AGE bovine serum albumin（AGE-BSA） at the concentration of 100,200 and 500 μg/ml for 24 hours in vitro,and a normal control group and a BSA group were established for comparison.The proliferation of the SW-480 cells was assessed by MTT assay,the cell cycles analyzed by flow cytometry,and the expressions of AGE receptor（RAGE） mRNA and cyclin D1 mRNA detected by real-time quantitative PCR.Results After treatment with 100,200 and 500 μg/ml AGE-BSA for 24 hours,the proliferation of the SW-480 cells was significantly increased in a dose-dependent manner（P0.05）.Compared with the normal control group,the proportion of the SW-480 cells was remarkably decreased in the G1 stage and increased in the S stage（P0.05）,and the expressions of RAGE mRNA and cyclin D1 mRNA in the SW-480 cells significantly enhanced by AGE-BSA at the concentration of 200 μg/ml（P0.05）.Conclusion AGEs can promote the proliferation of human colon carcinoma SW-480 cells,mainly by upregulating the expressions of RAGE mRNA and cyclin D1 mRNA and accelerating the cell cycle from the G1 to S stage.
出处
《医学研究生学报》
CAS
2010年第9期924-927,共4页
Journal of Medical Postgraduates
