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Keywords = quinolyl nitrones

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18 pages, 4559 KiB  
Article
Neuroprotective and Antioxidant Properties of CholesteroNitrone ChN2 and QuinolylNitrone QN23 in an Experimental Model of Cerebral Ischemia: Involvement of Necrotic and Apoptotic Cell Death
by Beatriz Chamorro, Sara Izquierdo-Bermejo, María Dolores Martín-de-Saavedra, Francisco López-Muñoz, Mourad Chioua, José Marco-Contelles and María Jesús Oset-Gasque
Antioxidants 2023, 12(7), 1364; https://doi.org/10.3390/antiox12071364 - 29 Jun 2023
Cited by 5 | Viewed by 2050
Abstract
Ischemic stroke is the leading cause of disability and the second leading cause of death worldwide. However, current therapeutic strategies are scarce and of limited efficacy. The abundance of information available on the molecular pathophysiology of ischemic stroke has sparked considerable interest in [...] Read more.
Ischemic stroke is the leading cause of disability and the second leading cause of death worldwide. However, current therapeutic strategies are scarce and of limited efficacy. The abundance of information available on the molecular pathophysiology of ischemic stroke has sparked considerable interest in developing new neuroprotective agents that can target different events of the ischemic cascade and may be used in combination with existing treatments. In this regard, nitrones represent a very promising alternative due to their renowned antioxidant and anti-inflammatory effects. In this study, we aimed to further investigate the neuroprotective effects of two nitrones, cholesteronitrone 2 (ChN2) and quinolylnitrone 23 (QN23), which have previously shown great potential for the treatment of stroke. Using an experimental in vitro model of cerebral ischemia, we compared their anti-necrotic, anti-apoptotic, and antioxidant properties with those of three reference compounds. Both ChN2 and QN23 demonstrated significant neuroprotective effects (EC50 = 0.66 ± 0.23 μM and EC50 = 2.13 ± 0.47 μM, respectively) comparable to those of homo-bis-nitrone 6 (HBN6) and N-acetylcysteine (NAC) and superior to those of α-phenyl-N-tert-butylnitrone (PBN). While primarily derived from the nitrones’ anti-necrotic capacities, their anti-apoptotic effects at high concentrations and antioxidant powers—especially in the case of QN23—also contribute to their neuroprotective effects. Full article
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
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24 pages, 4112 KiB  
Article
Preclinical Characterization of Antioxidant Quinolyl Nitrone QN23 as a New Candidate for the Treatment of Ischemic Stroke
by Emma Martínez-Alonso, Alejandro Escobar-Peso, Alicia Aliena-Valero, Germán Torregrosa, Mourad Chioua, Rocío Fernández-Serra, Daniel González-Nieto, Youness Ouahid, Juan B. Salom, Jaime Masjuan, José Marco-Contelles and Alberto Alcázar
Antioxidants 2022, 11(6), 1186; https://doi.org/10.3390/antiox11061186 - 16 Jun 2022
Cited by 8 | Viewed by 3139
Abstract
Nitrones are encouraging drug candidates for the treatment of oxidative stress-driven diseases such as acute ischemic stroke (AIS). In a previous study, we found a promising quinolylnitrone, QN23, which exerted a neuroprotective effect in neuronal cell cultures subjected to oxygen–glucose deprivation and in [...] Read more.
Nitrones are encouraging drug candidates for the treatment of oxidative stress-driven diseases such as acute ischemic stroke (AIS). In a previous study, we found a promising quinolylnitrone, QN23, which exerted a neuroprotective effect in neuronal cell cultures subjected to oxygen–glucose deprivation and in experimental models of cerebral ischemia. In this paper, we update the biological and pharmacological characterization of QN23. We describe the suitability of intravenous administration of QN23 to induce neuroprotection in transitory four-vessel occlusion (4VO) and middle cerebral artery occlusion (tMCAO) experimental models of brain ischemia by assessing neuronal death, apoptosis induction, and infarct area, as well as neurofunctional outcomes. QN23 significantly decreased the neuronal death and apoptosis induced by the ischemic episode in a dose-dependent manner and showed a therapeutic effect when administered up to 3 h after post-ischemic reperfusion onset, effects that remained 11 weeks after the ischemic episode. In addition, QN23 significantly reduced infarct volume, thus recovering the motor function in a tMCAO model. Remarkably, we assessed the antioxidant activity of QN23 in vivo using dihydroethidium as a molecular probe for radical species. Finally, we describe QN23 pharmacokinetic parameters. All these results pointing to QN23 as an interesting and promising preclinical candidate for the treatment of AIS. Full article
(This article belongs to the Special Issue Pharmacology of Antioxidants)
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