Publications by authors named "Irene Bulli"

3 Publications

  • Page 1 of 1

Protective Effect of Adenosine A Receptor Agonist, BAY60-6583, Against Transient Focal Brain Ischemia in Rat.

Front Pharmacol 2020 11;11:588757. Epub 2021 Feb 11.

Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Division of Pharmacology and Toxicology, University of Florence, Florence, Italy.

Cerebral ischemia is a multifactorial pathology characterized first by an acute injury, due to excitotoxicity, followed by a secondary brain injury that develops hours to days after ischemia. During ischemia, adenosine acts as an endogenous neuroprotectant. Few studies have investigated the role of A receptor in brain ischemia because of the low potency of adenosine for it and the few selective ligands developed so far. A receptors are scarcely but widely distributed in the brain on neurons, glial and endothelial cells and on hematopoietic cells, lymphocytes and neutrophils, where they exert mainly anti-inflammatory effects, inhibiting vascular adhesion and inflammatory cells migration. Aim of this work was to verify whether chronic administration of the A agonist, BAY60-6583 (0.1 mg/kg i.p., twice/day), starting 4 h after focal ischemia induced by transient (1 h) Middle Cerebral Artery occlusion (tMCAo) in the rat, was protective after the ischemic insult. BAY60-6583 improved the neurological deficit up to 7 days after tMCAo. Seven days after ischemia BAY60-6583 reduced significantly the ischemic brain damage in cortex and striatum, counteracted ischemia-induced neuronal death, reduced microglia activation and astrocytes alteration. Moreover, it decreased the expression of TNF-α and increased that of IL-10 in peripheral plasma. Two days after ischemia BAY60-6583 reduced blood cell infiltration in the ischemic cortex. The present study indicates that A receptors stimulation can attenuate the neuroinflammation that develops after ischemia, suggesting that A receptors may represent a new interesting pharmacological target to protect from degeneration after brain ischemia.
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http://dx.doi.org/10.3389/fphar.2020.588757DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905306PMC
February 2021

New Insight into the Role of Adenosine in Demyelination, Stroke and Neuropathic Pain.

Front Pharmacol 2020 29;11:625662. Epub 2021 Jan 29.

Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, Florence, Italy.

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http://dx.doi.org/10.3389/fphar.2020.625662DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7878385PMC
January 2021

A Adenosine Receptors: When Outsiders May Become an Attractive Target to Treat Brain Ischemia or Demyelination.

Int J Mol Sci 2020 Dec 18;21(24). Epub 2020 Dec 18.

Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Section of Pharmacology and Toxicology, University of Florence, 50139 Florence, Italy.

Adenosine is a signaling molecule, which, by activating its receptors, acts as an important player after cerebral ischemia. Here, we review data in the literature describing AR-mediated effects in models of cerebral ischemia obtained in vivo by the occlusion of the middle cerebral artery (MCAo) or in vitro by oxygen-glucose deprivation (OGD) in hippocampal slices. Adenosine plays an apparently contradictory role in this receptor subtype depending on whether it is activated on neuro-glial cells or peripheral blood vessels and/or inflammatory cells after ischemia. Indeed, ARs participate in the early glutamate-mediated excitotoxicity responsible for neuronal and synaptic loss in the CA1 hippocampus. On the contrary, later after ischemia, the same receptors have a protective role in tissue damage and functional impairments, reducing inflammatory cell infiltration and neuroinflammation by central and/or peripheral mechanisms. Of note, demyelination following brain ischemia, or autoimmune neuroinflammatory reactions, are also profoundly affected by ARs since they are expressed by oligodendroglia where their activation inhibits cell maturation and expression of myelin-related proteins. In conclusion, data in the literature indicate the ARs as putative therapeutic targets for the still unmet treatment of stroke or demyelinating diseases.
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http://dx.doi.org/10.3390/ijms21249697DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7766015PMC
December 2020