ArticleJournal of advanced research2025
Plasma-activated solutions prevent peritoneal adhesion formation by regulating eNOS expression in mesothelial cells.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Aspirin prevents postoperative peritoneal adhesions by inhibiting the TGF‑β1/Smad signaling pathway in rats.Molecular medicine reports · 2026Article
- Gastric cancer-secreted galectin-1 promotes peritoneal mesothelial-mesenchymal transition to prime peritoneal metastasis soil.iScience · 2026Article
- Cellular and molecular regulation of fibrotic postoperative abdominal adhesions.American journal of physiology. Cell physiology · 2026Review
- Plasma-activated solutions reverse chronic deltamethrin exposure induced intestinal injury via rebalancing redox homeostasis and counteracting cellular senescence.Scientific reports · 2026Article
- Inhibitory effects of cold atmospheric plasma-activated solution on cutaneous squamous cell carcinoma.Frontiers in pharmacology · 2026Article
- HMGB1-enhanced autophagic degradation of E-cadherin facilitates mesothelial trans-differentiation and postoperative peritoneal adhesion.BMC gastroenterology · 2025Article
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPeritoneal adhesions cause significant morbidity due to limited therapeutic options. Current strategies are limited by inconsistent efficacy and potential side effects. Plasma-activated solutions (PAS) exhibit anti-inflammatory and healing promoting properties with good safety, their efficacy in preventing peritoneal adhesions remains further investigation.
objectivesThis study aimed to investigate the therapeutic potential of PAS in preventing peritoneal adhesion formation and to elucidate its mechanisms.
methodsTwo murine peritoneal adhesion models ("ischemic button" and "cecum-peritoneum abrasion") were established. Human peritoneal mesothelial cell was treated with LPS or TGF-β1 to model apoptosis and mesothelial-to-mesenchymal transition (MMT) in vitro. Apoptosis was quantified via flow cytometry and western blotting; ROS levels were assessed using immunofluorescence staining. MMT markers (western blotting) and inflammatory cytokines (ELISA) were analyzed. Histological evaluation included Masson's trichrome and immunofluorescence staining.
resultsPAS-2 min significantly reduced adhesion scores compared to PBS controls (ischemic button: 6.250 ± 1.389 vs. 2.5 ± 2.268; abrasion: 7.333 ± 1.033 vs. 1.633 ± 1.333, p < 0.01). In vitro, PAS treatment decreased LPS-induced apoptosis in mesothelial cells by 8.14 % (flow cytometry: 39.10 % ± 1.47 % vs. 30.96 % ± 1.73 %, p < 0.01) and suppressed MMT markers, with N-cadherin and Vimentin expression reduced by 1.46-fold (p < 0.05) and 1.62-fold (p < 0.05). PAS also attenuated oxidative stress, decreasing general ROS levels by 3-fold (p < 0.001) and mitochondrial ROS (mtROS) by 2-fold (p < 0.01). Mechanistically, reactive nitrogen species (RNS) in PAS restored eNOS expression, attenuating apoptosis and MMT in mesothelial cells.
conclusionThis study demonstrates that PAS prevents peritoneal adhesions via RNS-mediated eNOS restoration, suppressing oxidative stress, apoptosis, and MMT. These findings position PAS as a novel and promising therapy for adhesion prevention, warranting clinical translation.
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