Effect of diallyl disulfide on the expression and secretion of VEGF in HL-60 cells.
- Author:
Zi-Li FAN
1
;
Zhen-Hua QI
;
Yi XIE
Author Information
- Publication Type:Journal Article
- MeSH: Allyl Compounds; pharmacology; Antineoplastic Agents; pharmacology; Disulfides; pharmacology; Dose-Response Relationship, Drug; HL-60 Cells; Humans; RNA, Messenger; biosynthesis; Reverse Transcriptase Polymerase Chain Reaction; Vascular Endothelial Growth Factor A; biosynthesis; drug effects; secretion
- From: Chinese Journal of Hematology 2006;27(9):626-629
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the proliferation inhibition of human leukemic cell line HL-60 and the expression of vascular endothelial growth factor (VEGF) mRNA and secretion of VEGF protein in HL-60 cells treated with diallyl disulfide (DADS).
METHODSMTT was used to test the cell growth, semi-quantitative RT-PCR and ELISA to study the expression of VEGF mRNA and secretion of VEGF protein.
RESULTSDADS significantly inhibited proliferation of HL-60 cell and the inhibiting effects showed a dose (r > 0.9, P < 0.01) and time-dependent( r > 0.7, P < 0.01) manner. The expression of VEGF mRNA and secretion of VEGF protein could be down regulated by 0.625, 1.250, and 2.500 microg/mL DADS in HL-60 cells for 24,48 and 72 hours exposure and the effects also showed dose -dependence(r > 0.9, P < 0.01). The growth inhibition rates of DADS in HL-60 cells at three dosages for 24 hours were (8.19 +/- 3.34)%, (16.79 +/- 2.07)% and (21.30 +/- 2.72)%, those for 48 hours were (11.93 +/- 3.93)%, (22.81 +/- 2.31)% and (30.74 +/- 2.03)%, for 72 hours were (16.68 +/- 2.37)%, (28.54 +/- 3.26)% and (36.59 +/- 2.37)% respectively, The difference between the DADS-treated and untreated HL-60 cells was statistically significant (P < 0.01). There were also statistically significant differences among the three groups of different dosages (P < 0.01).
CONCLUSIONDADS can effectively inhibit the proliferation of HL-60 cells. DADS probably exerts its anti-leukemia effects by reducing the expression of VEGF mRNA and secretion of VEGF protein in HL-60 cells.