Interferon ? and plasminogen activator inhibitor 1 regulate adhesion formation after partial hepatectomy  

Oleh:

Ohashi, K. ; Yoshimoto, T. ; Kosaka, H. ; Hirano, T. ; Iimuro, Y.

Jenis: Article from Article - diterbitkan di jurnal ilmiah internasional
Dalam koleksi: BJS: British Journal of Surgery vol. 101 no. 04 (Mar. 2014), page 398–407.

Ketersediaan

Perpustakaan FK Nomor Panggil: B15.K.2014.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background The pathophysiology of intra-abdominal adhesions has not been studied extensively. The aim of this study was to elucidate the molecular mechanisms underlying adhesion formation in a murine model and in patients undergoing hepatectomy. Methods Partial hepatectomy was performed using bipolar forceps in mice. Wild-type mice, antibodies to CD4 and interferon (IFN) ?, IFN-?, natural killer T (NKT) cells and plasminogen activator inhibitor (PAI) 1 knockout (KO) mice were used. Recombinant hepatocyte growth factor (HGF) was tested for its ability to prevent adhesions. Liver specimens were obtained during surgery from patients undergoing hepatectomy. Adhesion formation was evaluated using a scoring system that ranged from 0 (no adhesions) to 5 (severe adhesions). Levels of IFN-? and PAI-1 mRNA, and protein concentration of PAI-I were measured, and fluorescence immunostaining was performed. Results Adhesion formation depended on IFN-? produced by NKT cells, and NKT KO mice developed few adhesions (mean(s.d.) 1·7(0·3) versus 4·6(0·4) in wild-type mice; P?=?0·037). In wild-type mice, the level of PAI-1 mRNA increased after hepatectomy, followed by a decrease in the tissue plasminogen activator (tPA) mRNA level. Adhesion formation was inhibited completely in PAI-1 KO mice (0(0) versus 4·1(0·8) in wild-type mice; P?=?0·002). HGF inhibited formation of abdominal adhesions after hepatectomy by reducing IFN-? and PAI-1 levels, and increasing tPA levels compared with those in mice treated with phosphate-buffered saline (P?

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