Design, Synthesis and Biological Evaluation of a Novel Sulfonamide Derivative as antiproliferative agents for Human Breast Cancer Cell line (MCF-7)
Volume 12, Issue 2, Winter 2022, Pages 91-102
Mohaddeseh Baravordeh, Hossein Ghafouri, Asadollah Mohammadi, Sevda Zarei
Abstract Aim: During the uncontrolled development of cells in the body, a subset of neoplasms or tumors is formed, the abnormal proliferation of these cells leads to the formation of a mass and eventually cancer. This mass can spread throughout the body. Thus, inhibiting the abnormal growth of cancer cells will have a significant effect on preventing the spread of cancerous tumors and improving the disease. Therefore, in the present study, a new sulfonamide derivative was designed and synthesized (HB20) and its anti-cancer effects on human breast cancer cell line (MCF-7) were investigated.
Materials and Methods: For the synthesis of a sulfonamide derivative (HB20), dcriptiazonium salt was first made using a sulfamethoxazole base compound and then combined with a pyrimidine coupling agent. Concentrations of a new synthetic compound (HB20) against Cells (MCF-7) were used. MTT assay was also performed to measure survival and cell proliferation.
Results: The synthesized compound structure was confirmed by spectral analysis, such as FT- IR, and NMR. Also, Survival in MCF-7 cells treated with a synthetic compound (HB20) was significantly reduced compared to the control group (untreated). HB20 inhibits the proliferation of MCF-7 cancer cells with an IC50 value of 75/23 μg/ml.
Conclusion: The new sulfonamide derivative (HB20) has the potential to inhibit proliferation and anti-cancer properties in the cell line (MCF-7).
Effect of Electromagnetic Field and Nitric Oxide on the Neural Differentiation Proteins Marker and Viability of the Rat Bone Marrow Mesenchymal Stem Cells
Volume 9, Issue 3, Summer 2018, Pages 459-464
N. Haghighat, P. Abdolmaleki, M. Behmanesh, J. Parnian
Abstract Aims: Nitric oxide (NO) plays an important role in maintaining cellular stem status, and the range of electromagnetic fields (EMF) is very deep in contrast to the electric field. The aim of this study was to investigate the effect of electromagnetic field and nitric oxide on the neural differentiation proteins marker and viability of the rat bone marrow mesenchymal stem cells.
Materials and Methods: The present experimental research was conducted on bone marrow mesenchymal stem cells of Vistar rats. For treatments of the cells, high (1mM) and low (10micromolar Deta-NO) concentrations were used as a nitric oxide donor molecule and 50Hz low-frequency electromagnetic field and they were compare with the control group. The cell viability was recorded by MTT assay test, the neural differentiation pathway gene expression was investigated by RT-PCR technique, and the neural differentiation marker protein expression was evaluated by Immunocytochemistry technique. The data were analyzed by one-way ANOVA, using SPSS 13 software.
Findings: After 24 hours of treatment with nitric oxide and EMF, the rate of viability in all groups was significantly decreased compared to the control group. After 48 hours, EMF alone, as well as with low concentration of nitric oxide did not decrease the rate of viability and cell growth increased compared to the control group. In the group treated with high nitric oxide concentration along with EMF, MAP2 protein was expressed in the number of cells more than the control group and the one treated with EMF.
Conclusion: The electromagnetic field, along with its high concentration of nitric oxide, decreases the number of rat bone marrow mesenchymal stem cells and, by increasing cell size, gene expression and neural differentiation proteins marker facilitates their differentiation to nerve-like cells.
Investigation of apoptosis induction through caspase 9 activation by silibinin in Human Umbilical Vein Endothelial Cells (HUVEC)
Volume 7, Issue 2, Spring 2016, Pages 20-30
hosein ghafoori
Abstract Abstract- Silibinin a natural flavonoid has been reported to induce cell death in various types of cancers and also in endothelial cells which shows its anti-angiogenesis effect. However, its molecular mechanism is not clearly defined. In this article, we provided evidence for one of the mechanisms by which Silibinin induces apoptosis in HUVEC. For this purpose, HUVECs were grown on 96 well plates and cell viability was measured by MTT assay and IC50 was determined as 143μM after 24 hr of treatment by Silibinin. Caspase-9 activity in dose dependent (100-300μM) and time dependent (24,48 and 72hr) treatment by Silibinin was assessed using chromogenic substrate LEHD-pNA. Maximum activity of caspase 9 was in 100 μM of silibinin after 48 hours of treatment. DNA fragmentation was analyzed by gel electrophoresis. Cells were incubated with different concentrations of silibinin (100-400μM) and DNA that was extracted from cells which were incubated by 400 μM of silibinin formed a smear on agarose gel. Data obtained from this study showed the ability of Silibinin to inhibit HUVEC cell proliferation through apoptosis induction which indicates the anti-angiogenesis effect of this compound.
