ABSTRACT
Lymphoma-associated hemophagocytic syndrome (LAHS) accounts for a large proportion of secondary hemophagocytic syndrome (HPS) and has a poor prognosis. LAHS can be divided into two categories: HPS combined with chemotherapy and lymphoma-induced HPS. The key to the treatment of HPS combined with chemotherapy is to control the infection. While the treatment of lymphoma-induced HPS is complicated, there are new strategies in addition to traditional methods. Timely and appropriate treatment can significantly improve the short-term and long-term prognosis of patients. This article summarizes the progress in treatment of LAHS.
ABSTRACT
This study investigated the inhibitory effects of curcumin on proliferation of hematological malignant cells in vitro and the anti-tumor mechanism at histone acetylation/histone deacetylation levels. The effects of curcumin and histone deacetylase inhibitor trichostatin A (TSA) on the growth of Raji cells were tested by MTT assay. The expression of acetylated histone-3 (H(3)) in Raji, HL60 and K562 cells, and peripheral blood mononuclear cells (PBMCs) treated with curcumin or TSA was detected by immunohistochemistry and FACS. The results showed curcumin inhibited proliferation of Raji cells significantly in a time- and dose-dependent fashion, while exhibited low toxicity in PBMCs. Curcumin induced up-regulation of the expression of acetylated H(3) dose-dependently in all malignant cell lines tested. In conclusion, curcumin inhibited proliferation of Raji cells selectively, enhanced the level of acetylated (H(3)) in Raji, HL60, and K562 cells, which acted as a histone deacetylase inhibitor like TSA. Furthermore, up-regulation of H(3) acetylation may play an important role in regulating the proliferation of Raji cells.
Subject(s)
Acetylation/drug effects , Antineoplastic Agents/pharmacology , Cell Proliferation/drug effects , Curcumin/pharmacology , HL-60 Cells , Histone Deacetylase Inhibitors/pharmacology , Histones/chemistry , Histones/drug effects , K562 Cells , Triclosan/pharmacologyABSTRACT
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 histone_3 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.Curcumin at the concertration of 25 ?mol?L~(-1) could enhance acetylated histones in the three tumor cells(P