Objective: To 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).
Methods: MTT 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.
Results: DADS 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).
Conclusion: DADS 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.
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Molecules
December 2024
Laboratory of Advanced Materials in Biopharmaceutics and Technics, Institute of Chemistry, Moldova State University, MD-2009 Chisinau, Moldova.
Ten coordination compounds, [Cu(L)Cl] (), [Cu(L)NO] (), [Cu(L)Cl] (C3), [Cu(L)NO] (), [Cu(L)Cl] (), [Cu(L)NO] (), [Cu(L)NO] (), [Cu(L)Cl] (), [Cu(L)Cl] (), and [Cu(L)NO] (), containing pyridine derivatives of -methoxyphenyl-thiosemicarbazones were synthesized and characterized. The molecular structure of four compounds was investigated using single crystal X-ray diffraction. Spectral analysis techniques such as FT-IR, H NMR, C NMR, elemental analysis, and molar conductivity were used for all the synthesized compounds.
View Article and Find Full Text PDFChem Pharm Bull (Tokyo)
January 2025
Faculty of Pharmaceutical Sciences, Teikyo University, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
Life Sci
January 2025
Department of Biological Sciences (Regulatory Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, TS 500037, India. Electronic address:
Pulmonary fibrosis (PF) arises from dysregulated wound healing, leading to excessive extracellular matrix (ECM) deposition and impaired lung function. Macrophages exhibit high plasticity, polarizing to pro-inflammatory M1 during early inflammation and anti-inflammatory, fibrosis-inducing M2 during later stages of PF. Additionally, neutrophils and neutrophil extracellular traps (NETs) release mediated by peptidyl arginine deiminase (PAD-4), also play a key role in PF progression.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
Department of Biological Medicines & Shanghai Engineering Research Center of Immunotherapeutics, School of Pharmacy, Fudan University, Shanghai 201203, China.
Acute myeloid leukemia (AML) is a severe blood cancer with an urgent need for novel therapies for refractory or relapsed patients. Leukocyte-associated immunoglobulin-like receptor 1 (LAIR1), an immune suppressive receptor expressed on immune cells and AML blasts but minimally on hematopoietic stem cells (HSCs), represents a potential therapeutic target. But there has been limited research on therapies targeting LAIR1 for AML and no published reports on LAIR1 antibody-drug conjugate (ADC).
View Article and Find Full Text PDFZhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Department of Oncology, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi Province, China.
Objective: To investigate the effects of Curcumol on the malignant biological characteristics of acute myeloid leukemia (AML) cells and its molecular mechanism, and to provide theoretical and experimental evidence for the anti-leukemia treatment of traditional Chinese medicine.
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