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用于腹膜内植入修补的脱细胞人羊膜改良生物复合补片的评估

Evaluation of a Biocomposite Mesh Modified with Decellularized Human Amniotic Membrane for Intraperitoneal Onlay Mesh Repair.

作者信息

Liu Zhengni, Zhu Xiaoqiang, Zhu Tonghe, Tang Rui

机构信息

Department of Hernia and Abdominal Wall Surgery, Shanghai East Hospital, Tongji University, 150 Ji Mo Road, Shanghai 200120, P. R. China.

Department of Sports Medicine, Medicine and Department of Orthopedics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No. 600 Yishan Road, Shanghai 200233, P. R. China.

出版信息

ACS Omega. 2020 Feb 13;5(7):3550-3562. doi: 10.1021/acsomega.9b03866. eCollection 2020 Feb 25.

DOI:10.1021/acsomega.9b03866
PMID:32118170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7045508/
Abstract

Various materials and approaches have been used to optimize the biocompatibility of mesh to reduce the implant-induced host response in intraperitoneal onlay mesh (IPOM) repair. Ineffective host integration, limited resistance to contamination, and untargeted administration hinder the wider application of the currently available clinical options. In this study, human amniotic membrane (HAM) was decellularized, fully characterized, and compared with porcine small intestinal submucosa (SIS) in terms of its structure, components, and bioactivity. In an in vivo study, HAM was reinforced with silk fibroin (SF) membrane, which was fabricated as a biodegradable submicroscale template by electrospinning, to construct a bilayer composite mesh. The independent SF membrane, associated with HAM and SIS, was evaluated for tissue remodeling in vitro. The HAM-SF and SIS meshes were then characterized morphologically and implanted intraperitoneally into Sprague-Dawley rats for 28 days for macroscopic investigation of their integration into the host via interactions of regulatory factors. After decellularization, HAM formed a bioagent-rich collagen-based acellular structure. HAM was superior to SIS in concurrently suppressing the expression of transforming growth factor β1 (TGF-β1) and proangiogenic proliferation. When HAM, SF, and SIS were used as regenerative scaffolds, they showed qualified biocompatibility, cell infiltration, and degradation in vitro. Comparatively, macroscopic observation after implantation indicated that HAM-SF induced less-intensive intraperitoneal adhesion and weaker inflammatory responses at the interface but greater angiogenesis in the explant than SIS. Analysis of the expression of regulatory factors showed a greater quantity of hepatocyte growth factor (HGF) in HAM, which partly inhibited the expression of TGF-β1 and promoted vascular endothelial growth factor (VEGF)-induced angiogenesis. This bioactive interaction appeared to be responsible for the better host integration, making HAM more biocompatible than SIS in IPOM repair. When combined with SF, HAM displayed similar mechanical properties to SIS. In conclusion, HAM displayed better bioactivity and biocompatibility than SIS. After its reinforcement with SF, HAM-SF is a promising biocomposite mesh for IPOM repair.

摘要

为优化补片的生物相容性以减少腹腔内植入补片(IPOM)修复中植入物引起的宿主反应,人们使用了各种材料和方法。宿主整合效果不佳、抗污染能力有限以及给药缺乏针对性阻碍了当前临床可用方案的广泛应用。在本研究中,对人羊膜(HAM)进行了脱细胞处理、全面表征,并在结构、成分和生物活性方面与猪小肠黏膜下层(SIS)进行了比较。在一项体内研究中,用丝素蛋白(SF)膜增强HAM,该膜通过静电纺丝制成可生物降解的亚微米级模板,以构建双层复合补片。对与HAM和SIS相关的独立SF膜进行体外组织重塑评估。然后对HAM - SF和SIS补片进行形态学表征,并将其腹腔内植入Sprague - Dawley大鼠体内28天,通过调节因子的相互作用对它们与宿主的整合进行宏观研究。脱细胞后,HAM形成了富含生物因子的基于胶原蛋白的无细胞结构。在同时抑制转化生长因子β1(TGF - β1)的表达和促血管生成增殖方面,HAM优于SIS。当HAM、SF和SIS用作再生支架时,它们在体外表现出合格的生物相容性、细胞浸润和降解能力。相比之下,植入后的宏观观察表明,与SIS相比,HAM - SF诱导的腹腔内粘连强度较低,界面处炎症反应较弱,但植入物中的血管生成更强。调节因子表达分析表明,HAM中肝细胞生长因子(HGF)的含量更高,这部分抑制了TGF - β1的表达并促进了血管内皮生长因子(VEGF)诱导的血管生成。这种生物活性相互作用似乎是更好的宿主整合的原因,使HAM在IPOM修复中比SIS具有更高的生物相容性。与SF结合时,HAM表现出与SIS相似的机械性能。总之,HAM比SIS表现出更好的生物活性和生物相容性。用SF增强后,HAM - SF是一种有前途的用于IPOM修复的生物复合补片。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/1ce8e9578088/ao9b03866_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/ddbf437c5b96/ao9b03866_0008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/99b59e569126/ao9b03866_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/1cf2070a92d7/ao9b03866_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/1ce8e9578088/ao9b03866_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/ddbf437c5b96/ao9b03866_0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/c0239e974dbd/ao9b03866_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/14219a634018/ao9b03866_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/cf9a8247e521/ao9b03866_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/99b59e569126/ao9b03866_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/1cf2070a92d7/ao9b03866_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7017/7045508/1ce8e9578088/ao9b03866_0004.jpg

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