Analysis of the effectiveness and risk benefit of N acetyl cysteine compared to ceftriaxone in the expression of GLT1 transporters.

• Guzmán-Priego, Crystell Guadalupe ; Benitez Arias, Hafiz ^[1] ; Granados Villalpando, Jesus Maximilano ^[1] ; Totosau Betancourt, Liliana ^[1]
  1. [1] Universidad Juárez Autónoma de Tabasco

     Universidad Juárez Autónoma de Tabasco

     México

     
• Localización: Emerging Trends in Education, ISSN-e 2594-2840, Vol. 7, Nº. 1, 2022 (Ejemplar dedicado a: Multidisciplinary Health Research)
• Idioma: inglés
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• Resumen

  • The concentration of glutamate in the synaptic cleft is regulated primarily by glutamate transporters, especially by the glial glutamate-specific transporter type 1 (GLT-1). Ceftriaxone (CTX), a β-lactam antibiotic, has been reported to significantly increase GLT-1 expression. N-acetylcysteine ​​as a derivative of cysteine, is oxidized into cystine within the brain, increasing the availability of cystine for the glial cystine-glutamate exchanger, this action increases the amount of glutamate exchanged by glial cells, raising the concentration of glutamate within the extra-synaptic space and effectively promoting GLT-1 transcription. It is suspected that the β-lactam antibiotic ceftriaxone is more effective than N-acetylcysteine ​​in upregulating GLT-1 expression. We conducted a systematic review to investigate the effectiveness of the drugs N-acetylcysteine ​​and ceftriaxone with respect to their effect on increasing the expression of GLT-1 transporters in experimental studies. This systematic review was carried out with methodology in accordance with the Cochrane Handbook and reporting consistent with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The main objective of this work is to determine the difference in effectiveness of N-acetylcysteine compared to Ceftriaxone in the expression of the GLT-1 transporter. A clear superiority is shown by ceftriaxone, because by itself it can induce an increase in the levels of these proteins either in circumstances where the glutamatergic flux is affected or in control groups, in contrast to N-acetylcysteine. which improves the expression of these transporters only when there is a deficit in the levels of GLT-1.