Cellular & Molecular Biology Letters | |
The effects of disodium pamidronate on human polymorphonuclear leukocytes and platelets: An in vitro study | |
Arianna Vignini2  Laura Mazzanti2  Eleonora Salvolini1  Monia Orciani1  Roberto Primio1  | |
[1] Department of Molecular Pathology and Innovative Therapies - Histology, Polytechnic University of Marche, Ancona, Italy$$;Institute of Biochemistry, Polytechnic University of Marche, Ancona, Italy$$ | |
关键词: Pamidronate; Polymorphonuclear leukocytes; Platelets; Nitric oxide; Intracellular calcium; Myeloperoxidase activity; | |
DOI : 10.2478/s11658-009-0012-6 | |
学科分类:分子生物学,细胞生物学和基因 | |
来源: Uniwersytet Wroclawski * Wydzial Biotechnologii / University of Wroclaw, Faculty of Biotechnology | |
【 摘 要 】
Recent reports have indicated that, as well as having antiresorptive effects, bisphosphonates could have an application as anti-inflammatory drugs. Our aim was to investigate whether this anti-inflammatory action could be mediated by the nitric oxide (NO) released by the leukocytes migrating to the site of inflammation. In particular, we investigated in vitro the intracellular calcium concentration ([Ca2+]i), the level of NO released by PMN and platelets, and the PMN myeloperoxidase activity after incubation with disodium pamidronate, since there was a postulated modulatory effect of this aminosubstituted bisphosphonate on leukocytes both in vitro and in vivo. Our data shows that the pamidronate treatment provoked a significant increase in the [Ca2+]i parallel to the enhancement in NO release, suggesting a possible activation of constitutive nitric oxide synthase, while the myeloperoxidase activity was significantly reduced. In conclusion, we hypothesized that treatment with pamidronate could stimulate NO-production by cells present near the bone compartment, thus constituting a protective mechanism against bone resorption occurring during inflammation. In addition, PMN- and platelet-derived NO could act as a negative feed-back signal to restrict the inflammatory processes.
【 授权许可】
Unknown
【 预 览 】
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