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天然水蛭素通过PARs/p38/NF-κB途径抗炎增加大鼠皮瓣存活率。

Natural Hirudin Increases Rat Flap Viability by Anti-Inflammation via PARs/p38/NF-κB Pathway.

作者信息

Peng Liu, Pan Xinyuan, Yin Guoqian

机构信息

Guangxi Medical University, Nanning, Guangxi 530021, China.

Department of Plastic and Aesthetic Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.

出版信息

Biomed Res Int. 2015;2015:597264. doi: 10.1155/2015/597264. Epub 2015 Dec 7.

DOI:10.1155/2015/597264
PMID:26770977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4685076/
Abstract

The present study aimed to evaluate the effect of natural hirudin on rat random skin flap viability and to determine the mechanism. Forty-eight rats were randomly divided into 2 groups. After the dorsal skin flap operation (3 cm × 10 cm in size), subcutaneous injections of 6 ATU hirudin were administered to group H (n = 24) every 12 h, while group C (n = 24) received an equal volume of 0.9% normal saline. Six rats from each group were euthanized 1, 2, 4, and 7 days after the operation. A full skin sample was collected from these rats to measure the p38-mitogen-activated protein kinase (p38-MAPK), phospho-p38- (Pp38-) MAPK, nuclear factor-κB (NF-κB) p65, phosphor-NF-κB (pNF-κB) p65, tumour necrosis factor- (TNF-) α, interleukin- (IL-) 6, and intercellular adhesion molecule- (ICAM-) 1 levels via western blot (WB) assays. The results showed that flap viability was significantly higher in the hirudin-treated group, which showed a reduced inflammatory response compared with the control group. The Pp38/p38, pNF-κB p65/NF-κB p65, TNF-α, IL-6, and ICAM-1 levels in the hirudin-treated group were lower than those in the control group. The results demonstrated that hirudin could improve random skin flap viability and suggested that this effect maybe occurs by blocking the thrombin/proteinase-activated receptors (PARs)/p38/NF-κB signalling pathway, thus decreasing the inflammatory response.

摘要

本研究旨在评估天然水蛭素对大鼠随意皮瓣存活能力的影响并确定其机制。48只大鼠被随机分为两组。在进行背部皮瓣手术(尺寸为3 cm×10 cm)后,H组(n = 24)每12小时皮下注射6个抗凝血酶单位(ATU)的水蛭素,而C组(n = 24)接受等体积的0.9%生理盐水。术后1、2、4和7天,每组处死6只大鼠。从这些大鼠身上采集全层皮肤样本,通过蛋白质免疫印迹(WB)分析来测量p38丝裂原活化蛋白激酶(p38-MAPK)、磷酸化p38-(Pp38-)MAPK、核因子-κB(NF-κB)p65、磷酸化核因子-κB(pNF-κB)p65、肿瘤坏死因子-(TNF-)α、白细胞介素-(IL-)6和细胞间黏附分子-(ICAM-)1的水平。结果显示,水蛭素治疗组的皮瓣存活能力显著更高,与对照组相比炎症反应减轻。水蛭素治疗组的Pp38/p38、pNF-κB p65/NF-κB p65、TNF-α、IL-6和ICAM-1水平低于对照组。结果表明,水蛭素可提高随意皮瓣的存活能力,并提示这种作用可能是通过阻断凝血酶/蛋白酶激活受体(PARs)/p38/NF-κB信号通路,从而减轻炎症反应实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/a49028570407/BMRI2015-597264.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/07be012eff91/BMRI2015-597264.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/54dddc0a8589/BMRI2015-597264.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/5fe7feecc318/BMRI2015-597264.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/a49028570407/BMRI2015-597264.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/07be012eff91/BMRI2015-597264.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/54dddc0a8589/BMRI2015-597264.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/5fe7feecc318/BMRI2015-597264.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f936/4685076/a49028570407/BMRI2015-597264.004.jpg

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