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  • 1.
    Fjæraa Alfredsson, Christina
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Ding, Menglei
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Liang, Qiu-Li
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Sundström, Birgitta
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Nånberg, Eewa
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Ellagic acid induces a dose- and time-dependent depolarization of mitochondria and activation of caspase-9 and -3 in human neuroblastoma cells2014In: Biomedicine and Pharmacotherapy, ISSN 0753-3322, E-ISSN 1950-6007, Vol. 68, no 1, p. 129-135Article in journal (Refereed)
    Abstract [en]

    The polyphenol ellagic acid is found in many natural food sources and has been proposed as a candidate compound for clinical applications due to its anti-oxidative capacity and as a potential anti-tumorigenic compound. The objective of the present study was to evaluate the sensitivity to and possible apoptosis mechanism induced by ellagic acid in neuronal tumor cells. As a model the human neuroblastoma SH-SY5Y cell line was used. The methods applied were bright field and phase contrast microscopy, XTT- and LDH-assays, western blot, and flow cytometric analysis of DNA degradation and mitochondrial membrane potential. Ellagic acid treatment was found to induce a reduction in cell number preceded by alterations of the mitochondrial membrane potential and activation of caspase-9 and -3, DNA-fragmentation and cell death by apoptosis. The apoptotic cell death studied was not due to anoikis since it was significant in the adherent fraction of the cells. We conclude that ellagic acid induces dose- and time-dependent apoptosis, at least partly by the mitochondrial pathway, in an embryonal neuronal tumor cell system. This finding is in agreement with previously reported data on adult carcinoma cells thus suggesting a more general effect of ellagic acid on tumor cells.

  • 2.
    Fjæraa Alfredsson, Christina
    et al.
    Biomedical Sciences, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden.
    Rendel, Filip
    Biomedical Sciences, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden.
    Liang, Qui-Li
    Biomedical Sciences, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden.
    Sundström, Birgitta E
    Biomedical Sciences, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden.
    Nånberg, Eewa
    Biomedical Sciences, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden.
    Altered sensitivity to ellagic acid in neuroblastoma cells undergoing differentiation with 12-0-tetradecanoylphorbol-13-acetate and all-trans retinoic acid2015In: Biomedicine and Pharmacotherapy, ISSN 0753-3322, E-ISSN 1950-6007, Vol. 76, p. 39-45Article in journal (Refereed)
    Abstract [en]

    Ellagic acid has previously been reported to induce reduced proliferation and activation of apoptosis in several tumor cell lines including our own previous data from non-differentiated human neuroblastoma SH-SY5Y cells. The aim of this study was now to investigate if in vitro differentiation with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate or the vitamin A derivative all-trans retinoic acid altered the sensitivity to ellagic acid in SH-SY5Y cells. The methods used were cell counting and LDH-assay for evaluation of cell number and cell death, flow cytometric analysis of SubG(1)-and TUNEL-analysis for apoptosis and western blot for expression of apoptosis-associated proteins. In vitro differentiation was shown to reduce the sensitivity to ellagic acid with respect to cell detachment, loss of viability and activation of apoptosis. The protective effect was phenotype-specific and most prominent in all-trans retinoic acid-differentiated cultures. Differentiation-dependent up-regulation of Bcl-2 and integrin expression is introduced as possible protective mechanisms. The presented data also point to a positive correlation between proliferative activity and sensitivity to ellagic-acid-induced cell detachment. In conclusion, the presented data emphasize the need to consider degree of neuronal differentiation and phenotype of neuroblastoma cells when discussing a potential pharmaceutical application of ellagic acid in tumor treatment.

  • 3.
    Fjæraa Alfredsson, Christina
    et al.
    Karlstads universitet, Institutionen för hälsovetenskaper (from 2013).
    Rendel, Filip
    Karlstads universitet, Institutionen för hälsovetenskaper (from 2013).
    Sundström, Birgitta E.
    Karlstads universitet, Institutionen för hälsovetenskaper (from 2013).
    Nånberg, Eewa
    Karlstads universitet, Institutionen för hälsovetenskaper (from 2013).
    Proliferation in morphologically differentiated SH-SY5Y human neuroblastoma cellsManuscript (preprint) (Other academic)
  • 4.
    Rendel, Filip
    et al.
    Biomedical Sciences, Karlstad University, Karlstad, Sweden.
    Fjaeraa Alfredsson, Christina
    Biomedical Sciences, Karlstad University, Karlstad, Sweden.
    Bornehag, Carl-Gustaf
    Public Health Science, Department of Health Sciences, Faculty of Health, Science and Technology, Karlstad University, Karlstad, Sweden; Icahn School of Medicine at Mount Sinai, New York, NY, USA.
    Sundström, Birgitta E.
    Biomedical Sciences, Karlstad University, Karlstad, Sweden.
    Nånberg, Eewa
    Örebro University, School of Health Sciences. Biomedical Sciences, Karlstad University, Karlstad, Sweden.
    Effects of Di-Isononyl Phthalate on Neuropeptide Y Expression in Differentiating Human Neuronal Cells2017In: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 120, no 3, p. 218-323Article in journal (Refereed)
    Abstract [en]

    Neuropeptide Y (NPY) is an abundant neuropeptide in the mammalian brain important for behavioural consequences of stress and energy metabolism. We have addressed possible effects of the phthalate DiNP on NPY expression in human SH‐SY5Y cells, a neuronal in vitro differentiation model. Pico‐ to nanomolar doses of DiNP and its metabolite MiNP resulted in decreased NPY mRNA and peptide expression in retinoid‐differentiated cells. Thus, dys‐regulated NPY may be an adverse outcome for exposure to low doses of DiNP in human beings.

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