| Autor: |
Wang TT; Department of Hematology and Oncology, Southeast University Medical College, Jiangsu Province, China., Yan D, Chen BA, Wang J, Xia GH, Wang S, Cheng J, Ding JH, Bao W |
| Jazyk: |
čínština |
| Zdroj: |
Zhongguo shi yan xue ye xue za zhi [Zhongguo Shi Yan Xue Ye Xue Za Zhi] 2012 Apr; Vol. 20 (2), pp. 246-51. |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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