摘要
目的:研究反应停对HL -60细胞马利兰耐药的逆转作用。方法:低剂量马利兰反复刺激HL- 60细胞造成 HL -60马利兰耐药细胞株,联合应用反应停加马利兰观察反应停对马利兰耐药HL- 60细胞的逆转作用,并检测细胞谷 胱甘肽(GSH)、血管内皮生长因子(VEGF)和细胞色素C水平。结果:马利兰对HL 60细胞的IC50为5.44mmol/L,对 马利兰耐药HL 60细胞的IC50>100mmol/L;反应停单独应用对马利兰耐药HL 60细胞生长无影响,但能使马利兰对 马利兰耐药HL -60细胞的IC50降至14.34mmol/L,同时降低细胞GSH、VEGF和升高细胞色素C水平。结论:反应停 对HL- 60细胞马利兰耐药有逆转作用,其机制可能与降低细胞GSH、VEGF和升高细胞色素C水平有关。
Aim: To study the reverse effect of thalidomide on myleran-resistant HL-60 cells. Methods: Myleran-resistant HL-60 cells was prepared by stimulating repeatedly with low dose of myleran. Reverse effect of thalidomide on myleran-resistant HL-60 cells was observed by treatment with thalidomide combined with myleran.The levels of GSH,VEGF, and cytochrome C were measured. Results: IC_ 50 of myleran on normal HL-60 and myleran-resistant HL-60 were 5.44 mmol/L and >100 mmol/L, respectively. Thalidomide alone had no effect on growth of myleran-resistant HL-60 cells but reduced IC_ 50 of myleran to 14.34 mmol/L,decreased the levels of GSH and VEGF and increased the release of cytochrome C. Conclusion: Thalidomide can reverse myleran-resistant HL-60 and its mechanism might be related to reduction of GSH and VEGF and increase of cytochrome C.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2005年第2期300-302,共3页
Journal of Zhengzhou University(Medical Sciences)