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富含成纤维细胞生长因子-2的纳米纤维支架促进跟腱愈合:一项对比实验研究。

FGF-2 enriched nanofiber scaffold for advancing achilles tendon healing: a comparative experimental investigation.

作者信息

Turgut Necmettin, Cengiz Çallıoğlu Funda, Bayraktar Aytül, Savran Mehtap, Aşcı Halil, Gülle Kanat, Ünal Meriç

机构信息

Department of Orthopedics and Traumatology, Faculty of Medicine, Adana Dr. Turgut Noyan Research and Training Centre, Başkent University, Adana, Türkiye.

Department of Textile Engineering, Engineering Faculty, Süleyman Demirel University, Isparta, Türkiye.

出版信息

Front Surg. 2024 Oct 17;11:1424734. doi: 10.3389/fsurg.2024.1424734. eCollection 2024.

DOI:10.3389/fsurg.2024.1424734
PMID:39483374
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11524941/
Abstract

INTRODUCTION

Achilles tendon rupture is a common and debilitating injury that significantly impacts mobility and quality of life. Effective treatment options that promote faster and more complete healing are needed. Fibroblast growth factor-2 (FGF-2) has shown potential in enhancing tendon repair. This study aims to investigate the efficacy of FGF-2 in promoting tendon healing in a rat model of Achilles tendon rupture, providing insights into its potential as a therapeutic option.

MATERIALS AND METHODS

Forty-eight rat hind legs with complete Achilles tendon ruptures were divided into four equal groups: the Sham (S) group (tendon repair only), the Polymer (P) group (tendon repair with scaffold wrapping), the Produced FGF-2 (PF) group (scaffold coated with lab-produced FGF-2), and the Commercial FGF-2 (CF) group (scaffold coated with commercially sourced FGF-2). Histological analyses at two and four weeks post-surgery evaluated healing based on nuclear morphology, vascularity, fibril organization, inflammation, and adipogenesis.

RESULTS

At the end of the second week, no macroscopic healing was observed in one rat each from the S and P groups. By the end of the fourth week, macroscopic healing was observed in all groups. The S and P groups exhibited similarly severe fibril disorganization, pathological adipogenesis, and sustained inflammation, particularly at the fourth week. In contrast, the CF group demonstrated improved tendon healing with increased vascularity and extracellular matrix, lower inflammatory cell infiltration, and better fibril organization. Pathological adipogenesis was absent in the CF group, especially at the fourth week. The PF group showed comparable improvements at the second week but experienced a relapse by the 4th week, with increased inflammation and adipogenesis.

CONCLUSION

FGF-2 coated scaffolds significantly enhanced tendon healing in a rat Achilles tendon rupture model by improving fibril organization, increasing vascularity, and reducing inflammation and pathological adipogenesis. These findings suggest that FGF-2 could be a promising therapeutic option for accelerating tendon repair. Future perspectives on tendon repair will focus on enhancing FGF-2 delivery using innovative scaffolds, paving the way for more effective therapies and improved patient outcomes.

摘要

引言

跟腱断裂是一种常见且使人衰弱的损伤,会显著影响活动能力和生活质量。需要有效的治疗方案来促进更快、更完全的愈合。成纤维细胞生长因子-2(FGF-2)已显示出在增强肌腱修复方面的潜力。本研究旨在调查FGF-2在大鼠跟腱断裂模型中促进肌腱愈合的疗效,以深入了解其作为一种治疗选择的潜力。

材料与方法

48只后肢跟腱完全断裂的大鼠被分为四组,每组数量相等:假手术(S)组(仅进行肌腱修复)、聚合物(P)组(用支架包裹进行肌腱修复)、自制FGF-2(PF)组(支架涂有实验室自制的FGF-2)和商用FGF-2(CF)组(支架涂有市售的FGF-2)。术后两周和四周进行组织学分析,根据细胞核形态、血管生成、纤维组织、炎症和脂肪生成评估愈合情况。

结果

在第二周结束时,S组和P组各有一只大鼠未观察到宏观愈合。到第四周结束时,所有组均观察到宏观愈合。S组和P组表现出同样严重的纤维紊乱、病理性脂肪生成和持续炎症,尤其是在第四周。相比之下,CF组肌腱愈合得到改善,血管生成和细胞外基质增加,炎症细胞浸润减少,纤维组织更好。CF组没有病理性脂肪生成,尤其是在第四周。PF组在第二周显示出类似的改善,但在第四周出现复发,炎症和脂肪生成增加。

结论

涂有FGF-2的支架通过改善纤维组织、增加血管生成以及减少炎症和病理性脂肪生成,显著增强了大鼠跟腱断裂模型中的肌腱愈合。这些发现表明,FGF-2可能是加速肌腱修复的一种有前景的治疗选择。肌腱修复的未来展望将集中在使用创新支架增强FGF-2递送,为更有效的治疗和改善患者预后铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/f46c7350b9b5/fsurg-11-1424734-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/5283c6c8ad01/fsurg-11-1424734-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/21088ebe99a6/fsurg-11-1424734-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/0402f214b833/fsurg-11-1424734-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/370123cb247d/fsurg-11-1424734-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/ea6722b682b3/fsurg-11-1424734-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/f46c7350b9b5/fsurg-11-1424734-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/5283c6c8ad01/fsurg-11-1424734-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/21088ebe99a6/fsurg-11-1424734-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/0402f214b833/fsurg-11-1424734-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/370123cb247d/fsurg-11-1424734-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/ea6722b682b3/fsurg-11-1424734-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f78/11524941/f46c7350b9b5/fsurg-11-1424734-g006.jpg

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