ArticleInflammopharmacology2026
Topical selegiline accelerates cutaneous wound healing with phase-specific modulation of MAPK signaling.
Article in Inflammopharmacology, 2026. 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPersistent inflammation, impaired growth-factor signaling, dysregulated apoptosis, and altered signaling-pathway dynamics contribute to delayed cutaneous wound healing. Selegiline, an irreversible monoamine oxidase-B inhibitor with established transdermal delivery, may favorably modulate these interconnected processes within the wound microenvironment.
methodsMale Wistar rats (n = 90) underwent a full-thickness dorsal excisional wound (~ 25 × 16 mm; ~400 mm²) and were randomly assigned to receive daily administration of vehicle or topical selegiline (0.2%, 0.5%, 1%, or 2% w/w). Wound closure was assessed on Days 3, 8, and 14, and tissues were harvested for hematoxylin and eosin-based histopathological scoring; quantification of interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-β), apoptotic biomarkers, extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK) p38, and c-Jun N-terminal kinases (JNK) transcripts.
resultsTopical selegiline accelerated wound closure in a dose-dependent manner, with greatest efficacy at 1-2% (86.18% (1%) and 90.28% (2%)), compared with 70.58% in the vehicle group. Histopathology showed reduced inflammation and more advanced granulation/angiogenesis and collagen organization. Selegiline reduced the injury-associated elevation of IL-1β, IL-6, and TNF-α, particularly at later time points, and was associated with enhanced PDGF and TGF-β during proliferative/remodeling phases, shifted apoptosis toward a pro-survival profile, and produced phase-linked changes in ERK/JNK/p38 transcripts.
conclusionsTopical selegiline was associated with faster excisional wound repair, most consistently at 1-2%, by accelerating closure and coordinating inflammatory resolution, growth-factor recovery, apoptosis balance, and MAPK-related signaling across healing phases. These findings support further preclinical evaluation of topical selegiline, including mechanistic validation, local and systemic safety assessment, pharmacokinetic characterization, and investigation in impaired or chronic wound models.
Indexed as
Identifiers
42742908What Socratic 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 Socratic graph.