In Brief Objective: To assess whether polysaccharides isolated from fungi, Phellinus spp, could reduce the adhesion and abscess formation in a rat peritonitis model. Summary Background Data: Although polysaccharides from Phellinus spp is a well-known material with antiinflammatory properties, little is known regarding its ability to prevent intraperitoneal adhesions. We have assessed the adhesion- and abscess-reducing effect of polysaccharides from Phellinus gilvus (PG) and Phellinus linteus (PL) in a rat peritonitis model. Methods: In 60 SD rats, experimental peritonitis was induced using the cecal ligation and puncture model (CLP). Animals were randomly assigned to 5 groups; ringer lactate solution (RL group), polysaccharides from PG and PL (PG and PL group), hyaluronic acid (HA group), and carboxymethylcellulose (CMC group). Intraperitoneal adhesions and abscesses were noted at 7 day after CLP. RT-PCR assay for urokinase-type plasminogen activator (uPA), its cellular receptor (uPAR), tissue-type plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), and tumor necrosis factor (TNF)- α was performed to assess the cecal tissue. Results: Adhesion formation was significantly reduced in PG, PL, CMC, and HA groups (P < 0.001) compared with that in RL group. The incidence of abscesses was also significantly reduced in PG and PL groups (P < 0.05) compared with that in the RL group. The level of uPA, uPAR, tPA, and TNF-α was highly expressed in PG and PL group, as compared with the RL group. Conclusions: We concluded that PG and PL had significant adhesion- and abscess-reducing effects and may act by modulating fibrinolytic capacity of uPA and/or tPA produced from macrophages in a rat peritonitis model. Polysaccharides from fungi, Phellinus spp, is a well-known natural product with antiinflammatory properties. We assessed the adhesion- and abscess-reducing effect by the polysaccharides in a rat peritonitis model. It prevented adhesion and abscess formation and may act by modulating fibrinolytic capacity of urokinase-type plasminogen activator and/or tissue-type plasminogen activator produced from activated macrophages in infectious conditions.
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Bae et al. (2005) studied this question.
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