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腹膜炎中腹膜粘连的体外分析

In vitro analysis of peritoneal adhesions in peritonitis.

作者信息

Toh H, Torisu M, Shimura H, Kitsuki H, Uchiyama A, Itoh H, Ohsato K

机构信息

First Department of Surgery, University of Occupational and Environmental Health School of Medicine, Kitakyushu, Japan.

出版信息

J Surg Res. 1996 Feb 15;61(1):250-5. doi: 10.1006/jsre.1996.0112.

Abstract

Peritoneal adhesions due to peritonitis make surgery more difficult and may cause complications. Clarifying the formation mechanism of peritoneal adhesions could help identify methods useful for their prevention. We cultured mesothelial monolayers on plates and microcarriers to simulate the parietal and visceral peritoneum, respectively. We then investigated the effects of lipopolysacchride (LPS) and tumor necrosis factor (TNF) on the homologous adhesion of these mesothelial monolayers. There was no adhesion of mesothelial monolayers in the control medium. When monolayers were cultured with endotoxin (LPS), approximately 90% of the microcarriers adhered to the mesothelial microplate. Adhesions occurred at LPS concentrations of 10 ng/ml and increased linearly in a dose-dependent manner. Kinetic studies revealed that the mesothelial adhesion appeared at 12 hr, and that 90% of the microcarriers were adherent after 24 hr. Open intercellular spaces were observed after a 24-hr treatment with LPS. Scanning electron microscopy revealed that the mesothelial cells adhered to the naked glass. LPS also caused increased permeability of the mesothelial monolayer. TNF did not cause any significant adhesion. Through our experiments we were able to develop an in vitro model of peritoneal adhesion using peritoneal mesothelial cell culture. Endotoxin caused an increase in homologous adhesion of peritoneal mesothelial monolayers, which may correspond to the initial stage of peritoneal adhesion formation in peritonitis.

摘要

腹膜炎导致的腹膜粘连会使手术难度增加,并可能引发并发症。阐明腹膜粘连的形成机制有助于确定预防粘连的有效方法。我们分别在平板和微载体上培养间皮单层细胞,以模拟壁腹膜和脏腹膜。然后,我们研究了脂多糖(LPS)和肿瘤坏死因子(TNF)对这些间皮单层细胞同源性粘连的影响。在对照培养基中,间皮单层细胞没有发生粘连。当单层细胞与内毒素(LPS)一起培养时,约90%的微载体附着在间皮微孔板上。在LPS浓度为10 ng/ml时出现粘连,并呈剂量依赖性线性增加。动力学研究表明,间皮粘连在12小时出现,24小时后90%的微载体发生附着。用LPS处理24小时后,观察到细胞间出现开放间隙。扫描电子显微镜显示间皮细胞附着在裸露的玻璃上。LPS还导致间皮单层细胞的通透性增加。TNF未引起任何明显的粘连。通过我们的实验,我们利用腹膜间皮细胞培养建立了腹膜粘连的体外模型。内毒素导致腹膜间皮单层细胞的同源性粘连增加,这可能与腹膜炎中腹膜粘连形成的初始阶段相对应。

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