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晚期糖基化终产物损害损伤肌腱的修复:大鼠研究。

Advanced glycation end products impair the repair of injured tendon: a study in rats.

机构信息

Department of Geriatrics, Shanghai Fourth People's Hospital Affiliated to Tongji University, No.1279 Sanmen Road, Shanghai, 200434, China.

The Second Clinical Medical College, Lanzhou University, No. 82 Cuiyingmen, Chengguan District, Lanzhou City, 730030, Gansu Province, China.

出版信息

BMC Musculoskelet Disord. 2024 Sep 3;25(1):700. doi: 10.1186/s12891-024-07760-z.

DOI:10.1186/s12891-024-07760-z
PMID:39227794
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11370031/
Abstract

BACKGROUND

The AGEs levels in tissues of diabetics and elderly tend to be higher than in normal individuals. This study aims to determine the effects of AGEs on Achilles tendon repair.

MATERIALS AND METHODS

Thirty-six male eight-week-old Sprague Dawley rats were selected in this study. The rats were randomly divided into two experimental groups and a control group after the transection of the Achilles tendon. During the tendon repair, the experimental groups were injected around the Achilles tendon with 350mmol/L (low dose group) and 1000mmol/L (high dose group) D-ribose 0.2 ml respectively to increase the AGEs level, while in the control group were given the same amount of PBS. The injections were given twice a week for six weeks. Collagen-I, TNF-α, and IL-6 expression in the healed Achilles tendon was assessed. Additionally, macroscopic, pathological, and biomechanical evaluations of Achilles tendon repair were conducted.

RESULTS

The repaired Achilles tendons in the high dose group showed severe swelling and distinctive adhesions. The histological score went up with the increase of the AGEs in the Achilles tendon (p<0.001). TNF- α and IL-6 in the Achilles tendon increased (p<0.001, p<0.001), and the production of collagen-I decreased with the accumulation of AGEs in the repaired Achilles tendon (p<0.001). The tensile strength of Achilles tendon in the high dose group was impaired significantly.

CONCLUSION

In current study, the compromised tendon repair model induced by AGEs was successfully established in rat. The study demonstrated that AGEs significantly impair Achilles tendon repair.

摘要

背景

糖尿病患者和老年人的组织中的 AGEs 水平往往高于正常人。本研究旨在确定 AGEs 对跟腱修复的影响。

材料和方法

本研究选择了 36 只 8 周龄雄性 Sprague Dawley 大鼠。将这些大鼠随机分为两组实验组和一组对照组,在切断跟腱后。在修复跟腱时,实验组分别在跟腱周围注射 350mmol/L(低剂量组)和 1000mmol/L(高剂量组)D-核糖 0.2ml,以增加 AGEs 水平,而对照组给予等量 PBS。每周注射两次,持续六周。评估愈合跟腱中的胶原-I、TNF-α 和 IL-6 的表达。此外,还对跟腱修复进行了宏观、病理和生物力学评估。

结果

高剂量组修复的跟腱表现出严重肿胀和明显粘连。跟腱中 AGEs 的增加导致组织学评分升高(p<0.001)。TNF-α 和 IL-6 在跟腱中的表达增加(p<0.001,p<0.001),而胶原-I 的产生随着修复的跟腱中 AGEs 的积累而减少(p<0.001)。高剂量组的跟腱拉伸强度明显受损。

结论

在本研究中,成功建立了大鼠 AGEs 诱导的受损跟腱修复模型。研究表明,AGEs 显著损害跟腱修复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/7f61ee1d2715/12891_2024_7760_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/7e8c23130dee/12891_2024_7760_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/8836b350c646/12891_2024_7760_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/ff469c3ddaf8/12891_2024_7760_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/2b681707525f/12891_2024_7760_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/948b2daacafd/12891_2024_7760_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/7f61ee1d2715/12891_2024_7760_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/7e8c23130dee/12891_2024_7760_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/8836b350c646/12891_2024_7760_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/ff469c3ddaf8/12891_2024_7760_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/2b681707525f/12891_2024_7760_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/948b2daacafd/12891_2024_7760_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c066/11370031/7f61ee1d2715/12891_2024_7760_Fig6_HTML.jpg

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