ArticleMolecular neurobiology2021
The Protective Effect of PK-11195 on Cognitive Impairment in Rats Survived of Polymicrobial Sepsis.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Host gene expression analysis in the detection of bacterial and viral etiology in children hospitalized with a suspected severe infection.Communications medicine · 2026Article
- Effects of Treatment with Dexmedetomidine on Neurochemical and Cognitive Alterations Induced by Sepsis in an Animal Model.Journal of molecular neuroscience : MN · 2025Article
- Biomarkers of sepsis associated encephalopathy: a bibliometric and visualized analysis.Frontiers in neurology · 2025Article
- Identification of iron metabolism-related genes as diagnostic signatures in sepsis by blood transcriptomic analysis.Open life sciences · 2023Article
- Mitochondrial protective effects caused by the administration of mefenamic acid in sepsis.Journal of neuroinflammation · 2022Article
- A crosstalk between gut and brain in sepsis-induced cognitive decline.Journal of neuroinflammation · 2022Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is an organ dysfunction caused by a host's unregulated response to infection, causing long-term brain dysfunction with microglial activation, the release of inflammatory components, and mitochondrial changes. Neuroinflammation can increase the expression of the 18-kD translocator protein (TSPO) in the mitochondria, leading to the activation of the microglia and the release of inflammatory components. The antagonist PK-11195 can modulate TSPO and reduce microglial activation and cognitive damage presented in an animal model of sepsis. The aim of this was to evaluate the effects of PK-11195 on long-term brain inflammation and cognitive impairment in an animal model of sepsis. Wistar rats, 60 days old, were submitted to cecal ligation and puncture (CLP) surgery, divided into groups control/saline, control/PK-11195, sepsis/saline, and sepsis/PK-11195. Immediately after surgery, the antagonist PK-11195 was administered at a dose of 3 mg/kg. Ten days after CLP surgery, the animals were submitted to behavioral tests and determination of brain inflammatory parameters. The sepsis/saline group presented cognitive damage. However, there was damage prevention in animals that received PK-11195. Besides, the sepsis increased the levels of cytokines and M1 microglia markers and caused oxidative damage. However, PK-11195 had the potential to decrease inflammation. These events show that the modulation of neuroinflammation during sepsis by PK-11195, possibly related to changes in TSPO, improves mitochondrial function in the animals' brains. In conclusion, the antagonist PK-11195 attenuated brain inflammation and prevented cognitive impairment in animals subjected to sepsis.
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