Open AccessCurcumin, a potent anti‐tumor reagent, is a novel histone deacetylase inhibitor regulating B‐NHL cell line Raji proliferation 1
Author(s) -
LIU Hongli,
CHEN Yan,
CUI Guohui,
ZHOU Jianfeng
Publication year - 2005
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2005.00081.x
Subject(s) - raji cell , curcumin , microbiology and biotechnology , cell growth , histone deacetylase inhibitor , hdac3 , apoptosis , histone deacetylase , cell culture , hdac8 , chemistry , histone deacetylase 5 , biology , cancer research , cell , biochemistry , histone , genetics , gene
Aim: To investigate curcumin (diferuloylmethane) induced apoptosis and its molecular mechanism of action in B‐NHL cell line Raji cells. Methods: Raji cells were cultured in RPMI‐1640 medium and treated with curcumin in different concentrations. 3‐(4,5‐Dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2 H ‐tetrazolium (MTT) assay was used to detect growth inhibition and Hoechst 33258 staining was used to detect apoptosis. Immunocytochemistry and Western blot were used to detect the expressions of histone deacetylase 1, 3, and 8 (HDAC1, HDAC3, and HDAC8) and acetylated histone H4 (Ac‐histone H4) protein. Results: Curcumin inhibited the proliferation of B‐NHL cell line Raji cells with a 36‐h IC 50 value of 24.1±2.0 μmol/L. Hoechst 33258 staining showed that curcumin could induce Raji cell apoptosis. The expression levels of HDAC1, HDAC3, and HDAC8 proteins were downregulated following curcumin treatment in Raji cells, whereas Ac‐histone H4 protein expression was upregulated after treatment with curcumin. Conclusion: Curcumin, as a new member of the histone deacetylase inhibitors, can inhibit the expression of class I HDACs (HDAC1, HDAC3, and HDAC8), and can increase the expression of Ac‐histone H4 in Raji cells. Curcumin plays an important role in regulating B‐NHL cell line Raji cell proliferation and apoptosis.