Synthesis and biological impacts of pollen shells/Fe3O4 nanoparticles composites on human MG-63 osteosarcoma cells

达皮 细胞凋亡 活力测定 分子生物学 碘化丙啶 化学 生物 生物化学 程序性细胞死亡
作者
Solmaz Zakhireh,Yadollah Omidi,Younes Beygi‐Khosrowshahi,Abolfazl Barzegari,Jaleh Barar,Khosro Adibkia
出处
期刊:Journal of Trace Elements in Medicine and Biology [Elsevier BV]
卷期号:71: 126921-126921 被引量:13
标识
DOI:10.1016/j.jtemb.2022.126921
摘要

Cell-adhesive surfaces play a pivotal role in biomedical engineering, as most biological reactions take place on surfaces. Pollen shell (PSh) ofPistacia vera L., as a new medical device, has previously been reported to cause cytotoxicity and apoptosis in MG-63 bone cancer cells.Iron oxide nanoparticles (Fe3O4NPs) were synthesized and their reaction to PShs was gauged at different concentrations, and then characterized using field emission scanning electron microscopy (FESEM), Fourier-transform infrared spectroscopy, energy dispersion X-ray spectrometer, X-ray diffraction spectra, dynamic light scattering, and vibrating sample magnetometer. Then, the biological impacts of PShs/Fe3O4NPs composites on MG-63 cells were investigated in-vitro using MTT assay, quantitative polymerase chain reaction (qPCR), Annexin V/propidium iodide, FESEM, and DAPI staining.Fe3O4NPs with a size range of 24-40 nm and a zeta potential value of -37.4 mV were successfully assembled on the PShs. The viability of MG-63 cells was significantly decreased when cultured on the magnetic PShs as compared to non-magnetic PShs, in Fe3O4 concentration and time-dependent manner. In contrast, magnetic PShs had a positive effect on the viability of normal human bone marrow-derived mesenchymal stem cells (hBM-MSCs). The analysis of apoptosis-related genes in cancer cells revealed that loading Fe3O4NPs on PShs increased expression of BAX/BCL2 and caspase-3 genes. The increased apoptotic activity of combined PShs/Fe3O4NPs was further confirmed by flow cytometric measurement, morphological analysis, and DAPI staining.The incorporation of Fe3O4NPs into PShs could effectively increase anticancer effects on MG-63 cells via the mitochondria-mediated apoptosis pathway, evident by upregulation of BAX/BCL2 ratio and caspase-3.
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