ArticleIranian journal of pharmaceutical research : IJPR
miR-146a-Enriched Extracellular Vesicles Attenuate Neuroinflammation and Promote Recovery After Ischemic Stroke.
Article in Iranian journal of pharmaceutical research : IJPR. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ischemic stroke triggers a strong neuroinflammatory response involving cytokines, which are fundamentally involved in tissue damage and repair. Objectives: The present study was designed to investigate the therapeutic potential of miR-146a-enriched extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSC-EVs) in a rat model of middle cerebral artery occlusion (MCAO). Methods: miR-146a was transfected into BMSCs using Lipofectamine 3000. Extracellular vesicles (EVs) were isolated from transfected BMSCs using ultracentrifugation. Thirty rats were randomly assigned to three groups (n = 10 per group): (1) Control (received FBS), (2) miR-control EVs (miR-NC), and (3) miR-146a-enriched EVs, administered intravenously post-ischemia. Neurological deficits were evaluated with the Bederson score, and cytokine levels, including tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin (IL)-6, IL-10, as well as transforming growth factor β (TGF-β), were measured in splenocyte culture and brain tissues using enzyme-linked immunoassay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR), respectively. The expression of Interleukin-1 Receptor-Associated Kinase 1 (IRAK1), Tumor Necrosis Factor Receptor-Associated Factor 6 (TRAF6), and nuclear factor kappa B (NF-κB) was also measured using RT-PCR. Results: Results showed that EVs enriched in miR-146a significantly decreased pro-inflammatory cytokines, TNF-α, IFN-γ, and IL-6, and increased anti-inflammatory markers, IL-10 and TGF-β, when compared with miR-control EVs and FBS-treated groups. miR-146a-EV-treated rats also displayed better Bederson scores, which reflected better neurological recovery. Results also demonstrated that miR-146a-enriched EVs downregulated IRAK1, TRAF6, and NF-κB signaling in ischemic brain tissue. Conclusions: These results indicate that miR-146a overexpression in BMSC-EVs can significantly inhibit neuroinflammation and promote functional improvement in ischemic stroke models, supporting its targeted therapeutic potential.
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.