ArticleJournal of inflammation research2025
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Circadian rhythm disruption affects cellular senescence through the BMAL1/CRY2/PER1 signaling pathway in periodontitis.Journal of molecular histology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Purpose: This study aimed to elucidate the dual-target anti-inflammatory and antioxidant mechanisms of Methods: The periodontitis animal model of SD rats was established by ligation combined with Porphyromonas gingivalis (Pg) stimulation. The rats were locally administered HME (0.25%, 0.5%, and 1%, 0.5 mL/twice/day) for 14 days. Inflammatory responses of alveolar bone, expression of osteogenic related biomarkers, and activation of Nrf2/NF-κB signaling pathway were detected. In addition, LPS induced human periodontal ligament cells (HPDLs) to measure the effect of HME on cell viability, inflammatory response, Nrf2/NF- κB pathway and oxidative stress. Results: HME administration demonstrated significant efficacy in a ligature-induced periodontitis rat model: serum pro-inflammatory cytokines (IL-1β, IL-2, IL-6, IL-18, GM-CSF, and ICAM1) decreased by 24.9-50.6% at high HME concentrations, while Th2-related factors IL-4/IL-13 returned to baseline levels. Histopathological analysis revealed that HME maintained gingival epithelial integrity and suppressed osteoclast activity in a dose-dependent manner by downregulating RANKL. Mechanistic studies indicated that HME attenuated NF-κB activation by reducing nuclear p65 protein (44.1%) and enhanced the Nrf2-mediated antioxidant response, normalizing oxidative stress markers (MDA decreased by 55.3%; SOD restored to 142.3 U/mg). In vitro experiments confirmed HME's cytocompatibility at concentrations below 200µg/mL and its resistance to LPS stimulation, reducing ROS overaccumulation by 16.46% through modulation of the Nrf2/NF-κB axis. Conclusion: HME inhibits the progression of periodontitis in rats by downregulating the expression of inflammatory factors, alleviating oxidative stress, and repairing the Nrf2/NF-κB signaling pathway.
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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.