【摘要】 本研究旨在探讨晚期糖基化终末产物(AGE)对K562及K562/A02细胞增殖的影响及汉防己甲素(Tet)对AGE诱导细胞增殖的干预作用,并初步探讨其可能机制。用CCK8法观察AGE对K562及K562/A02细胞增殖及Tet对AGE诱导细胞增殖的影响,流式细胞术检测细胞凋亡率及晚期糖基化终末产物受体(RAGE)的表达,并用半定量RT-PCR检测RAGE mRNA相对表达水平。结果显示:AGE可促进K562及K562/A02细胞增殖,呈浓度依赖性,0-48 h内细胞增殖随时间延长而增强,72 h增殖仍明显高于对照组;AGE上调两种细胞RAGE mRNA及其蛋白的表达,具有浓度依赖性;Tet与AGE共作用于K562及K562/A02细胞48 h,可通过诱导细胞凋亡抑制AGE促细胞增殖的作用,且呈浓度依赖性,但Tet对AGE诱导RAGE mRNA及其蛋白表达的增加未见明显影响。结论:AGE可促进K562及K562/A02细胞增殖,其机制可能与上调细胞RGAE mRNA及其蛋白的表达有关;Tet可抑制AGE诱导的K562及K562/A02细胞增殖,其机制可能与改变AGE诱导的RGAE mRNA及其蛋白表达增加无关。更多还原

【Abstract】 This study was aimed to investigate the effect of advanced glycosylation end products(AGE) on the proliferation of K562 and K562/A02 cells,the effect of tetrandrine(Tet) on proliferation of K562 and K562/A02 cells induced by AGE,and their mechanisms.The effects of AGE on proliferation of K562 and K562/A02 cells and Tet on the proliferation of AGE-induced K562 and K562/A02 cells were assayed by CCK8 kit,the apoptosis rate and the expression of receptor of advanced glycosylation end products(RAGE) in K562 and K562/A02 cells were determined by flow cytometry,the expression of RAGE mRNA was detected by semi-quantitative RT-PCR.The results showed that AGE could promote the proliferation of K562 and K562/A02 cells in a concentration-dependent manner,the cell proliferation was enhanced with time increasing in 0-48 h,and was higher than control group after 72 h.AGE up-regulated the RAGE mRNA and protein expressions of K562 and K562/A02 cells in a concentration-dependent manner.Treatment of Tet combined with AGE for 48 h could inhibit the proliferation of K562 and K562/A02 cells promoted by AGE in a concentration-dependent manner,which probably by inducing cell apoptosis,however,there was no obvious effect in the up-regulating expression of RAGE mRNA and protein induced by AGE.It is concluded that AGE can promote the proliferation of K562 and K562/A02 cells,which is probably induced by up-regulating the expression of RAGE mRNA and protein.Tet can inhibit the proliferation of K562 and K562/A02 cells induced by AGE,and the mechanism may be not closely associated with changes of the up-regulating expression of RAGE mRNA and protein induced by AGE.更多还原