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Your search keyword '"FLORIO, SALVATORE"' showing total 8 results
Start Over Author "FLORIO, SALVATORE" Journal journal of cellular physiology
8 results on '"FLORIO, SALVATORE"'

3. Comparison of Dasatinib, Nilotinib, and Imatinib in the Treatment of Chronic Myeloid Leukemia

Author

Ciarcia, Roberto, primary, Damiano, Sara, additional, Puzio, Maria Valeria, additional, Montagnaro, Serena, additional, Pagnini, Francesco, additional, Pacilio, Carmen, additional, Caparrotti, Giuseppe, additional, Bellan, Cristiana, additional, Garofano, Tiziana, additional, Polito, Maria Sole, additional, Giordano, Antonio, additional, and Florio, Salvatore, additional

Published
2015
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4. Comparison of Dasatinib, Nilotinib, and Imatinib in the Treatment of Chronic Myeloid Leukemia.

Author

Ciarcia, Roberto, Damiano, Sara, Puzio, Maria Valeria, Montagnaro, Serena, Pagnini, Francesco, Pacilio, Carmen, Caparrotti, Giuseppe, Bellan, Cristiana, Garofano, Tiziana, Polito, Maria Sole, Giordano, Antonio, and Florio, Salvatore

Subjects
TREATMENT of chronic myeloid leukemia, DASATINIB, NILOTINIB, DRUG therapy, IMATINIB, DRUG resistance, PROTEIN-tyrosine kinase inhibitors, THERAPEUTICS
Abstract

To overcome the drug resistance phenomenon induced by Imatibib (IM), in clinical practice, are often used second generation of tyrosine kinase inhibitors as Nilotinib (NIL); a such potent inhibitor of the BCR/ABL kinase and Dasatinib (DAS), a inhibitor of BCR/ABL kinase, and inhibitor SrC family kinase. In this study we evaluated the in vivo effect of DAS, NIL, and IM on intracellular calcium concentration, oxidative stress, and apoptosis in peripheral blood leukocytes of 45 newly diagnosed patients with chronic myeloid leukaemia (CML-PBM). Our data demonstrated that treatment with DAS and NIL showed an higher modulating potential than IM on intracellular calcium concentration by inhibiting the thapsigargin, a sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) inhibitor, and Lithium (Li) an inositol 1,4,5-triphosphate (InsP3) receptor inhibitor activities. Moreover our data demonstrated that NIL and DAS have significantly increased apoptosis more than IM by involving both intracellular calcium signaling as well as oxidative stress. The acquisition of the oxidative stress and calcium channels receptors values data could help the hematologist to modulate and improve the treatment of chronic myeloid leukaemia (CML) pathology. J. Cell. Physiol. 231: 680-687, 2016. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Published
2016
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5. Imatinib treatment inhibit IL-6, IL-8, NF-KB and AP-1 production and modulate intracellular calcium in CML patients

Author

Ciarcia, Roberto, primary, Vitiello, Maria Teresa, additional, Galdiero, Massimiliano, additional, Pacilio, Carmen, additional, Iovane, Valentina, additional, d'Angelo, Danila, additional, Pagnini, David, additional, Caparrotti, Giuseppe, additional, Conti, Daniele, additional, Tomei, Valentina, additional, Florio, Salvatore, additional, and Giordano, Antonio, additional

Published
2012
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8. Hydrocortisone has a protective effect on CyclosporinA-induced cardiotoxicity

Author

F. Russo, Luca Crispino, Salvatore Florio, Christine Kumar, Ugo Pagnini, Antonio Ruocco, Giuseppina D'Andrilli, Roberto Ciarcia, Florio, Salvatore, Ciarcia, Roberto, Crispino, L., Pagnini, Ugo, Ruocco, A., Kumar, C., D'Andrilli, G., and Russo, Ferdinando

Subjects
Male, Hydrocortisone, Physiology, Clinical Biochemistry, chemistry.chemical_element, Pharmacology, Calcium, Nitric Oxide, Calcium in biology, Lipid peroxidation, chemistry.chemical_compound, Malondialdehyde, Calcium flux, Animals, Myocytes, Cardiac, Cells, Cultured, Calcium metabolism, Cardiotoxicity, Dose-Response Relationship, Drug, Cell Biology, Rats, Oxidative Stress, chemistry, Cytoprotection, Toxicity, Cyclosporine, Lipid Peroxidation, Immunosuppressive Agents, Intracellular
Abstract

CyclosporinA (CsA) is an immunosuppressive drug which induces severe adverse effects such as cardiotoxicity and nephrotoxicity. In several therapeutic protocols CsA is used in association with corticosteroids to obtain better therapeutic results. Recently, our studies showed that CsA increases blood pressure while inhibit Nitric Oxide (NO) production in vivo. In this study we evaluated in rat cardiomyocytes the effects of CsA, used alone or in association with Hydrocortisone (HY), on intracellular calcium concentration, NO production and lipid peroxidation (MDA level). Our results demonstrated that CsA increased intracellular calcium and such effect was dose-dependent. HY used alone, slightly decreased intracellular calcium, while dramatically reduced CsA-induced calcium fluxes. CsA (3.2 microM) increased lipid peroxidation and this effect was blunted by HY. Both CsA and HY inhibited NO production in rat cardiomyocytes acting on this pathway synergically. Our results demonstrated that in rat cardiomyocytes, CsA toxicity is due to a calcium overload, which in turn induce lipid peroxidation and determines oxidative stress-induced cell injury. Treatment with HY effectively inhibits CsA-induced toxicity, decreasing lipid peroxidation as well as calcium intracellular concentration. Our findings seem to suggest that glucocorticoids may be effective in reducing CsA-induced cardiotoxicity at concentrations which are consistent with current therapeutic doses.

Published
2003

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