期刊
NEUROTOXICITY RESEARCH
卷 38, 期 1, 页码 50-58出版社
SPRINGER
DOI: 10.1007/s12640-020-00192-2
关键词
Kynurenic acid; Striatum; Oxidative stress; Neuroinflammation; Na+; K+-ATPase; Acetylcholinesterase; Quinolinic acid
资金
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq-Brazil) [401507/2016]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) Brazil [EN 465671/2014-4]
- Fundacao de Amparo a Pesquisa do Rio Grande do Sul (FAPERGS) [16/2551-0000465-0]
Kynurenic acid (KYNA) and quinolinic acid (QUIN) are metabolites formed in the degradation of tryptophan (Trp). QUIN is a selective NMDA receptor antagonist and may exert neurotoxic effects, whereas KYNA is an agonist of glutamatergic and cholinergic receptors and presents antioxidant properties. KYNA/QUIN ratio is decreased in several central nervous system disorders, but the mechanisms involved are not well elucidated. In the present study, we try to determine the neuroprotective capacity of KYNA on the QUIN effects in redox homeostasis changes (H2DCF oxidation, superoxide dismutase/catalase (SOD/CAT) ratio, glutathione peroxidase (GPx) activity, sulfhydryl content, and nitrite levels), as well as on inflammatory parameters (levels of TNF-alpha, IL-1 beta, and IL-6). KYNA and QUIN effects on the activities of Na+,K+-ATPase and acetylcholinesterase (AChE) were also evaluated. Thirty-day-old male Wistar rats underwent stereotactic surgery and received intrastriatal injections as follows: group 1-control (PBS-injected), group 2-KYNA (100 mu M), group 3-QUIN (150 nM), and group 4-KYNA + QUIN (KYNA-injected followed QUIN-injected). Results demonstrated that the KYNA administration was able to prevent the increase in reactive oxygen species, SOD/CAT ratio, and pro-inflammatory cytokines (IL-1 beta and IL-6) and the decrease in GPx activity, sulfhydryl content, and nitrite levels caused by QUIN. KYNA was also able to partially prevent the decrease in Na+,K+-ATPase activity and the increase in AChE activity caused by QUIN. This study may help in the elucidation of neuroprotective effects of KYNA against oxidative and inflammatory insults caused by QUIN in the striatum of young male Wistar rats.
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