姜黄素诱导Raji、HL-60和K562组蛋白乙酰化的研究

Curcumin causes histone acetylation enhancement in Raji,HL-60 and K562 cell lines

目的研究姜黄素对淋巴瘤细胞系Raji细胞的抑制增殖作用,并在组蛋白乙酰化/去乙酰化水平对其抗肿瘤机制进行探讨。方法MTT法检测不同浓度姜黄素、TSA作用于Raji细胞的抑制增殖率。以TSA处理后的细胞为阳性对照,免疫组化法定量分析及免疫荧光流式细胞化学定量检测姜黄素作用后Raji、HL-60、K562细胞的组蛋白乙酰化H3水平。结果姜黄素抑制Raji细胞增殖,并呈时间剂量依赖性;25μmol.L-1姜黄素可致Raji、HL-60、K562细胞的乙酰化H3水平增加(P<0.05),50μmol.L-1姜黄素的诱导作用增强(P<0.01)。结论姜黄素可以选择性地抑制Raji细胞增殖;且类似于TSA诱导Raji,HL-60,K562细胞组蛋白乙酰化增加。

Aim To investigate whether the mechanism of curcumin antagonizing tumor correlates with histone acetylation/deacetylation, which is regarded as modulation of transcription level. Methods Measure the survival rates of Raji by treatment with various concentration of curcumin or TSA by the method of MTT; Measure the expression of acetylated histone3 in Raji, HL60 and K562 when treated with various concenration of curcumin or TSA by means of Immunohistochemistry and FACS. Results Curcumin could inhibit Raji cell proliferation in a time-dependent and dose-dependent manner. Cureumin at the eoneertration of 25 μmol · L^-1 could enhance aeetylated histones in the three tumor cells （ P 〈 0. 05 ） and the effects is more remarkable when the eoneertration is 50 μmol·L^-1 Conclusion eureumin could selectively inhibit Raji cell proliferation and induce histone aeetylation enhancement in Raji, HL60 and K562 cell, which is likeTSA.