ArticleMolecular medicine reports2026
Aspirin prevents postoperative peritoneal adhesions by inhibiting the TGF‑β1/Smad signaling pathway in rats.
Article in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Postoperative peritoneal adhesion (PPA) is a common complication following abdominal surgery and effective preventive strategies remain limited. The present study aimed to investigate the protective effect of aspirin against PPA in rats and to elucidate the underlying mechanism involving the transforming growth factor‑β1 (TGF‑β1)/Smad signaling pathway. A total of 32 male Sprague‑Dawley rats were randomly divided into the four following groups: Sham‑operated group, model group, low‑dose aspirin group (10 mg/kg) and high‑dose aspirin group (30 mg/kg). A PPA model was established by cecal wall abrasion. The aspirin‑treated groups received daily intragastric administration for 8 consecutive days post‑surgery. All animals were euthanized on day 8. Adhesion severity was assessed using the Nair scoring system; histopathological changes were examined by Masson's trichrome staining; the expression levels of proteins related to the TGF‑β1/Smad pathway and to markers of fibrosis were detected by western blot, immunohistochemical (IHC) and reverse transcription‑quantitative PCR (RT‑qPCR) analyses. In addition, rat primary peritoneal mesothelial cells (RPMCs) were treated with different concentrations of aspirin to evaluate the expression levels of the relevant proteins. The results indicated that compared with the model group, aspirin administration significantly reduced PPA scores. Histological examination revealed that aspirin treatment alleviated collagen deposition in adhesion tissues. The results derived from western blotting, IHC and RT‑qPCR analyses demonstrated that aspirin downregulated the expression levels of TGF‑β1, phosphorylated (p)‑Smad2/3, alpha smooth muscle actin (α‑SMA) and collagen type I, alpha 1 (COL1A1), and inhibited the phosphorylation of Smad2/3. Moreover, treatment of RPMCs with different concentrations of aspirin led to a dose‑dependent decrease in the protein expression levels of TGF‑β1, COL1A1, α‑SMA, p‑Smad2 and p‑Smad3, while simultaneously upregulating the expression levels of the endogenous inhibitory factor Smad6 in this pathway. In conclusion, the data demonstrated that aspirin effectively prevented the formation of PPA in rats by suppressing peritoneal fibrosis, an effect likely mediated via inhibition of the TGF‑β1/Smad signaling pathway. These findings suggest that aspirin is a promising candidate for the clinical prevention of PPA.
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