ArticleInflammopharmacology2016
Neurokinin-1 receptor inhibition reverses ischaemic brain injury and dementia in bilateral common carotid artery occluded rats: possible mechanisms.
Article in Inflammopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- The neuropeptide in ischemic brain injury: insights, challenges, and horizon of targeted interventions.Journal of translational medicine · 2026Pooled it
- Blockade of the SP/NK1 receptor axis: multimodal neuroprotection via inflammatory suppression, hypoxic modulation, and lympho-vascular remodeling in global cerebral ischemia.Metabolic brain disease · 2026Article
- Aprepitant's neuroprotective effects on methylphenidate-induced biochemical/mitochondrial dysfunction, neuroinflammation, and mood-related behavior alterations.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Review
- Aprepitant attenuates NLRC4-dependent neuronal pyroptosis via NK1R/PKCδ pathway in a mouse model of intracerebral hemorrhage.Journal of neuroinflammation · 2022Article
- Neurokinin Receptor 1 (NK1R) Antagonist Aprepitant Enhances Hematoma Clearance by Regulating Microglial Polarization via PKC/p38MAPK/NFκB Pathway After Experimental Intracerebral Hemorrhage in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Combined network pharmacology and virtual reverse pharmacology approaches for identification of potential targets to treat vascular dementia.Scientific reports · 2020Article
- Icariside II Ameliorates Cognitive Impairments Induced by Chronic Cerebral Hypoperfusion by Inhibiting the Amyloidogenic Pathway: Involvement of BDNF/TrkB/CREB Signaling and Up-Regulation of PPARα and PPARγ in Rats.Frontiers in pharmacology · 2018Article
- The role of substance P in epilepsy and seizure disorders.Oncotarget · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundsIncrease in SP release as a function of hypoxia of the rat carotid body is a tissue response to ischemia that leads to neurogenic inflammation and cognitive deficits. Substance P-mediated inflammation is reported to attenuate the neuroprotective PPAR-γ. This study was undertaken to investigate the effect of aprepitant, a substance P-NK1 receptor antagonist in bilateral carotid artery occlusion (BCCAO)-induced ischaemic brain injury and vascular dementia.
methodsBilateral carotid artery occlusion was performed in Wistar rats to produce hypoperfusion and ischaemic injury. Dementia was noted by an increase in brain acetylcholinesterase (AChE) activity, and attenuation of learning ability (escape latency time) and memory retention (time spent in target quadrant) using Morris water maze. Oxidative stress was estimated by an increase in thiobarbituric acid reactive substances (TBARS) level and a decrease in reduced glutathione level. Vascular dysfunction was measured by attenuation of acetylcholine-induced endothelium-dependent relaxation (isolated carotid ring preparation), and increased in carotid artery TBARS level. Neurodegeneration was assessed in the hippocampus by H&E staining. Aprepitant and donepezil (positive control) were administered to rats from day 28 to day 42 after BCCAO.
resultsAprepitant (20 and 40 mg/kg) and donepezil (2 mg/kg) significantly improved vascular function, learning and memory ability, and decreases the neuronal cell death, oxidative stress, and ache in BCCAO rats. Donepezil effect was more significant than the low dose of aprepitant on disease markers. However, BADGE (30 mg/kg a, PPAR-γ antagonist) prevented the ameliorative effect of aprepitant.
conclusionThus, it may be concluded that aprepitant attenuates vascular dysfunction and dementia in BCCAO rats by activating downstream PPAR-γ.
Indexed as
Identifiers
What OpenQuestion holds
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.