Prevention of intraperitoneal adhesions and abscesses by polysaccharides isolated from Phellinus spp in a rat peritonitis model.
OBJECTIVE
To assess whether polysaccharides isolated from fungi, Phellinus spp, could reduce the adhesion and abscess formation in a rat peritonitis model.


BACKGROUND
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)- alpha 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-alpha 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.
Bae
Jae-Sung
JS
Department of Surgery, College of Veterinary Medicine, Kangwon National University, Chunchon, Korea.
Ahn
So-Jeo
SJ
Yim
Hyunee
H
Jang
Kwang-Ho
KH
Jin
Hee Kyung
HK
D018784:Abdominal Abscess / Q000209:etiology / Q000382:microbiology / Q000517:prevention & control*; D000818:Animals; D001202:Ascitic Fluid / Q000382:microbiology; D001487:Basidiomycota; D002266:Carboxymethylcellulose Sodium / Q000627:therapeutic use; D002432:Cecum / Q000737:chemistry; D006820:Hyaluronic Acid / Q000627:therapeutic use; D008297:Male; D010538:Peritonitis / Q000150:complications* / Q000378:metabolism / Q000382:microbiology; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D011134:Polysaccharides / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011956:Receptors, Cell Surface / Q000032:analysis; D055293:Receptors, Urokinase Plasminogen Activator; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000267:Tissue Adhesions / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D010959:Tissue Plasminogen Activator / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014568:Urokinase-Type Plasminogen Activator / Q000032:analysis
D017395:Plasminogen Activator Inhibitor 1; C524900:Plaur protein, rat; D011134:Polysaccharides; D011956:Receptors, Cell Surface; D055293:Receptors, Urokinase Plasminogen Activator; D014409:Tumor Necrosis Factor-alpha; D006820:Hyaluronic Acid; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator; D002266:Carboxymethylcellulose Sodium
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