ArticleScientific reports2017
Cell-penetrating interactomic inhibition of nuclear factor-kappa B in a mouse model of postoperative cognitive dysfunction.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Pooled it
- Pooled it
- Value of narcotrend anesthesia depth monitoring in predicting POCD in gastrointestinal tumor anesthesia block patients.BMC anesthesiology · 2024Trial
- Oxygen, carbon dioxide, and nitric oxide: role in the pathophysiology of obstructive sleep apnea.Medical gas research · 2027Review
- Viral immunological complications in neurological surgery: A comprehensive review of homeostatic disturbances and cognitive impairments.Surgical neurology international · 2025Review
- Research progress of microglial surface receptors in perioperative neurocognitive disorders.Ibrain · 2024Review
- The involvement of the gut microbiota in postoperative cognitive dysfunction based on integrated metagenomic and metabolomics analysis.Microbiology spectrum · 2023Article
- The Impact of Persistent Noise Exposure under Inflammatory Conditions.Healthcare (Basel, Switzerland) · 2023Article
- METTL3 relieved the injury of SH-SY5Y cells treated with lipopolysaccharide and exposed to sevoflurane through regulating the m6A levels of Sox2.Brain and behavior · 2023Article
- Targeting neuroinflammation as a preventive and therapeutic approach for perioperative neurocognitive disorders.Journal of neuroinflammation · 2022Review
- Article
- Network Biology Approaches to Uncover Therapeutic Targets Associated with Molecular Signaling Pathways from circRNA in Postoperative Cognitive Dysfunction Pathogenesis.Journal of molecular neuroscience : MN · 2022Article
- Targeting the TLR4/NF-κΒ Axis and NLRP1/3 Inflammasomes by Rosuvastatin: A Role in Impeding Ovariectomy-Induced Cognitive Decline Neuropathology in Rats.Molecular neurobiology · 2022Article
- Neuroinflammation as the Underlying Mechanism of Postoperative Cognitive Dysfunction and Therapeutic Strategies.Frontiers in cellular neuroscience · 2022Review
- Cognitive impairment caused by hypoxia: from clinical evidences to molecular mechanisms.Metabolic brain disease · 2022Review
- TNF-α - mediated peripheral and central inflammation are associated with increased incidence of PND in acute postoperative pain.BMC anesthesiology · 2021Article
- Intranuclear Delivery of Nuclear Factor-Kappa B p65 in a Rat Model of Tooth Replantation.International journal of molecular sciences · 2021Article
- The relationship between inflammation and neurocognitive dysfunction in obstructive sleep apnea syndrome.Journal of neuroinflammation · 2020Review
- Inflammasome and Cognitive Symptoms in Human Diseases: Biological Evidence from Experimental Research.International journal of molecular sciences · 2020Review
- Bile duct ligation of C57BL/6 mice as a model of hepatic encephalopathy.Anesthesia and pain medicine · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some patients experience impaired cognitive functioning after surgery, a phenomenon referred to as postoperative cognitive dysfunction (POCD). Signs of POCD are closely associated with the development of systemic or hippocampal inflammation. However, the precise pathophysiological mechanisms of prevention/treatment options for POCD still remain unclear. After injury, the transcriptional factor nuclear factor-kappa B (NF-κB) is thought to regulate or stimulate inflammation amplification. Therefore, we designed a cell-penetrating fusion protein called nt-p65-TMD, which inhibits NF-κB p65 activation by translocating into the nucleus. In the present study, we discovered that nt-p65-TMD exerted effects on surgery-induced cognitive impairment in mice. Specifically, nt-p65-TMD exhibited strong immunoregulatory properties that were able to reduce surgery-induced elevations in cerebrovascular integrity impairment, subsequent peripheral immune-cell recruitment, and inflammation amplification, which ultimately lead to cognitive decline. The nt-p65-TMD has the unique ability to regulate and reduce systemic inflammation and inflammation amplification, suggesting a new strategy for preventing development of cognitive decline that occurs in POCD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.