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. 2023 Feb 14;18(2):e0281905.
doi: 10.1371/journal.pone.0281905. eCollection 2023.

Expression of Concern: Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

Expression of Concern: Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes

PLOS ONE Editors. PLoS One. .
No abstract available

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Figures

Fig 3
Fig 3. Histochemical alterations produced by QUIN in rats.
Peroxidase-based immunohistochemical staining of neuronal cells (NeuN) in striatal coronal sections (10X) of Sham (A, C and E)- and QUIN (B, D and F)- treated animals at different post-lesion times (Bar size 100 μm). Details of cell morphology for each treatment are shown in small squares (40X). The segmentation method was employed for cell counting, and expressed as immunopositive cells. In A, C and E, normal appearance of the striata with normal cell densities are shown. In B, D and F, the striatal appearance at 30, 60 and 120 min post-lesion is presented. Also in F, a considerable loss of neuronal density (indicated by arrow) can be appreciated close to the lesion site. In G, the numbers of immunopositive cells (mean percent ± SD), determined by the segmentation method, are graphically represented.

Expression of concern for

References

    1. Serratos IN, Castellanos P, Pastor N, Millán-Pacheco C, Rembao D, Pérez-Montfort R, et al.. (2015) Modeling the Interaction between Quinolinate and the Receptor for Advanced Glycation End Products (RAGE): Relevance for Early Neuropathological Processes. PLoS ONE 10(3): e0120221. 10.1371/journal.pone.0120221 - DOI - PMC - PubMed
    1. Rodríguez-Martínez E., Camacho A., Maldonado P. D., Pedraza-Chaverrí J., Santamaría D., Galván-Arzate S., & Santamaría A. (2000). Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum. Brain research, 858(2), 436–439. 10.1016/s0006-8993(99)02474-9 - DOI - PubMed
    1. Santamaría A., Galván-Arzate S., Lisý V., Ali S. F., Duhart H. M., Osorio-Rico L., Ríos C., & St’astný F. (2001). Quinolinic acid induces oxidative stress in rat brain synaptosomes. Neuroreport, 12(4), 871–874. 10.1097/00001756-200103260-00049 - DOI - PubMed
    1. Pérez-De La Cruz V., Konigsberg M., Pedraza-Chaverri J., Herrera-Mundo N., Díaz-Muñoz M., Morán J., Fortoul-van der Goes T., Rondán-Zárate A., Maldonado P. D., Ali S. F., & Santamaría A. (2008). Cytoplasmic calcium mediates oxidative damage in an excitotoxic /energetic deficit synergic model in rats. The European journal of neuroscience, 27(5), 1075–1085. 10.1111/j.1460-9568.2008.06088.x - DOI - PubMed
    1. Pérez-De La Cruz V., Elinos-Calderón D., Robledo-Arratia Y., Medina-Campos O. N., Pedraza-Chaverrí J., Ali S. F., & Santamaría A. (2009). Targeting oxidative/nitrergic stress ameliorates motor impairment, and attenuates synaptic mitochondrial dysfunction and lipid peroxidation in two models of Huntington’s disease. Behavioural brain research, 199(2), 210–217. 10.1016/j.bbr.2008.11.037 - DOI - PubMed

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