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发育内皮细胞定位-1 可预防小鼠腹膜粘连的形成。

Developmental endothelial locus-1 prevents development of peritoneal adhesions in mice.

机构信息

Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Department of Radiology and Research Institute of Radiology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2018 Jun 7;500(3):783-789. doi: 10.1016/j.bbrc.2018.04.158. Epub 2018 Apr 25.

Abstract

Postoperative peritoneal adhesions, fibrous bands formed in the peritoneal cavity following surgery, represent a common, challenging and costly problem faced by surgeons and patients, for which effective therapeutic options are lacking. Since aberrant inflammation is one of the key mechanisms underlying peritoneal adhesion formation, here we set out to study the role of developmental endothelial locus-1 (Del-1), which has been recently identified as an endogenous inhibitor of inflammation, in the formation of postoperative peritoneal adhesions using a mouse model of peritoneal adhesions induced by ischemic buttons. Del-1-deficient mice had a higher incidence of adhesions, and their adhesions had higher quality and tenacity scores. Del-1 deficiency also led to enhanced inflammation mediators and collagen production. Finally, Del-1 supplementation decreased the incidence and severity of postoperative peritoneal adhesions. Taken together, these results indicate a protective role for Del-1 in postoperative peritoneal adhesion formation.

摘要

术后腹膜粘连是手术后在腹膜腔内形成的纤维带,是外科医生和患者面临的一个常见、具有挑战性且代价高昂的问题,但目前缺乏有效的治疗选择。由于异常炎症是腹膜粘连形成的关键机制之一,因此我们着手使用由缺血纽扣诱导的腹膜粘连小鼠模型来研究发育内皮定位基因-1(Del-1)的作用,Del-1 最近被鉴定为炎症的内源性抑制剂。Del-1 缺陷小鼠的粘连发生率更高,其粘连的质量和韧性评分更高。Del-1 缺乏还导致炎症介质和胶原蛋白产生增加。最后,Del-1 补充减少了术后腹膜粘连的发生率和严重程度。总之,这些结果表明 Del-1 在术后腹膜粘连形成中起保护作用。

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