ArticleMetabolic brain disease2012
Antioxidant treatment prevents cognitive impairment and oxidative damage in pneumococcal meningitis survivor rats.
Article in Metabolic brain disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Melatonin Exerts Neuroprotective Effects in Escherichia coli/Lipopolysaccharide Induced Neuronal Injury via Regulating TFRC-Related Ferroptosis.Neurochemical research · 2026Article
- Review
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Cerebroprotective Effects of 2-Ethyl-6-methyl-3-hydroxypyridine-2,6-dichlorophenyl(amino)phenylethanoic Acid in the Treatment of Purulent Meningitis.Biomedicines · 2021Article
- Neuroinflammation trajectories precede cognitive impairment after experimental meningitis-evidence from an in vivo PET study.Journal of neuroinflammation · 2020Article
- Edaravone attenuates hippocampal damage in an infant mouse model of pneumococcal meningitis by reducing HMGB1 and iNOS expression via the Nrf2/HO-1 pathway.Acta pharmacologica Sinica · 2016Article
- Role of Microglial Activation in the Pathophysiology of Bacterial Meningitis.Molecular neurobiology · 2016Review
- Does Infection-Induced Immune Activation Contribute to Dementia?Aging and disease · 2015Review
- Nitrone-based therapeutics for neurodegenerative diseases: their use alone or in combination with lanthionines.Free radical biology & medicine · 2013Review
- Role of oxidative stress in the pathophysiology of pneumococcal meningitis.Oxidative medicine and cellular longevity · 2013Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pneumococcal meningitis is associated with the highest fatality case ratios in the world. Most of patients that survive present neurologic sequelae at later times as well as biochemicals alterations such as oxidative stress in both earlier and later times after central nervous system infection. In this context, we evaluated the effect of antioxidant treatment on memory and oxidative parameters in the hippocampus of meningitis survivor rats 10 days after infection. To this aim, the animals underwent a magna cistern tap receiving either 10 μL sterile saline as a placebo or an equivalent volume of a Streptococcus pneumoniae suspension at the concentration 5x10(9) cfu/mL. The animals submitted to meningitis were divided into the following groups: 1) treated with antibiotic, 2) treated with basic support plus N-acetylcysteine, 3) treated with basic support plus deferoxamine, 4) treated with basic support plus N-acetylcysteine and deferoxamine, or 5) treated with N-acetylcysteine plus deferoxamine. Ten days after meningitis, the animals underwent inhibitory avoidance and habituation to an open field tasks and, immediately after, were assessed for oxidative damage in the hippocampus and cortex. The meningitis group showed significantly decreased performance in latency retention compared with the sham group in the inhibitory avoidance task. In the open-field task, the meningitis group presented memory impairment after meningitis. All these memory impairments were prevented by N-acetylcysteine plus deferoxamine with or without basic support and its isolate use. In addition, there was an increase of lipid phosphorylation in cortex and hippocampus and all the combined antioxidants attenuated lipid phosphorylation in both structures. On the other hand, there was an increase of protein phosphorylation in cortex and N-acetylcysteine plus deferoxamine with or without basic support prevented it. Thus, we hypothesize that oxidative stress may be related to cognitive impairment in pneumococcal meningitis.
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