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本文引用的文献

1
Use of an IL1-receptor antagonist to prevent the progression of tendinopathy in a rat model.在大鼠模型中使用白细胞介素-1受体拮抗剂预防肌腱病进展。
J Orthop Res. 2016 Apr;34(4):616-22. doi: 10.1002/jor.23057. Epub 2015 Dec 29.
2
Effects of interleukin-1 receptor antagonist on collagen and matrix metalloproteinases in stress-shielded achilles tendons of rats.白细胞介素-1受体拮抗剂对大鼠应力屏蔽跟腱中胶原蛋白和基质金属蛋白酶的影响。
Orthopedics. 2012 Aug 1;35(8):e1238-44. doi: 10.3928/01477447-20120725-26.
3
Effect of prostaglandin E2 injection on the structural properties of the rat patellar tendon.前列腺素E2注射对大鼠髌腱结构特性的影响。
Sports Med Arthrosc Rehabil Ther Technol. 2012 Jan 9;4(1):2. doi: 10.1186/1758-2555-4-2.
4
A study on the mechanisms involving the anti-inflammatory effect of amitriptyline in carrageenan-induced paw edema in rats.一项关于阿米替林在角叉菜胶诱导的大鼠足肿胀中抗炎作用机制的研究。
Eur J Pharmacol. 2011 Sep 30;667(1-3):396-401. doi: 10.1016/j.ejphar.2011.05.053. Epub 2011 Jun 1.
5
Autologous tenocyte therapy for experimental Achilles tendinopathy in a rabbit model.兔实验性跟腱病模型中自体腱细胞治疗。
Tissue Eng Part A. 2011 Aug;17(15-16):2037-48. doi: 10.1089/ten.TEA.2010.0492. Epub 2011 Jun 10.
6
Animal models of tendinopathy.肌腱病的动物模型。
Disabil Rehabil. 2008;30(20-22):1530-41. doi: 10.1080/09638280701785460.
7
Coordinate regulation of IL-1beta and MMP-13 in rat tendons following subrupture fatigue damage.大鼠肌腱亚急性疲劳损伤后白细胞介素-1β和基质金属蛋白酶-13的协同调节
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8
Serum and tissue cytokines and chemokines increase with repetitive upper extremity tasks.血清和组织中的细胞因子及趋化因子会随着重复性上肢任务而增加。
J Orthop Res. 2008 Oct;26(10):1320-6. doi: 10.1002/jor.20674.
9
Increased IL-1beta expression and myofibroblast recruitment in subacromial bursa is associated with rotator cuff lesions with shoulder stiffness.肩峰下囊内白细胞介素-1β表达增加和成肌纤维细胞募集与伴有肩部僵硬的肩袖损伤相关。
J Orthop Res. 2008 Aug;26(8):1090-7. doi: 10.1002/jor.20631.
10
Novel procedure for high-fidelity tendon histology.高保真肌腱组织学的新方法。
J Orthop Res. 2007 Mar;25(3):390-5. doi: 10.1002/jor.20304.

利用白介素 1 受体拮抗剂逆转大鼠模型中与既定腱病相关的变化。

The use of an IL1-receptor antagonist to reverse the changes associated with established tendinopathy in a rat model.

机构信息

Department of Orthopaedics, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina.

出版信息

Scand J Med Sci Sports. 2019 Jan;29(1):82-88. doi: 10.1111/sms.13310. Epub 2018 Oct 15.

DOI:10.1111/sms.13310
PMID:30256459
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6289890/
Abstract

Interleukin-1 (IL1) is a cytokine that plays a role in inflammation and is a potential contributor to the inflammation present in tendinopathy. Its inhibition may be of use in the treatment of tendinopathy and has been a target for treatment. To evaluate how an IL1-receptor antagonist (IL1-RA) reverses pathologic changes associated with established patellar tendinopathy, we randomized 48 Sprague-Dawley retired breeder rats into three groups having weekly bilateral patellar tendon injections for 6 weeks. The control group received 0.1 mL saline for 6 weeks. The intervention groups were treated with 0.1 mL 2% carrageenan for 4 weeks. Beginning at week three, the IL1-RA group received 0.94 mg of the IL1-RA (2.5 mg/kg) added to the 0.1 mL 2% carrageenan and 0.94 mg of the IL1-RA alone for the final 2 weeks, while the CAR received 0.1 mL saline for the final 2 weeks. Animals were euthanized 6 weeks after initial injection. The CAR group demonstrated significantly (P < 0.05) shorter tendon lengths (7.81 ± 0.44 mm) than the control (8.25 ± 0.58 mm) and IL1-RA (8.34 ± 0.52 mm) group (P < 0.05). Macroscopically, plaque-like formations were reduced and margins of the tendon were more evident in the IL1-RA group compared to the CAR group. CAR group demonstrated significantly greater histopathologic changes (inflammatory cell density, disorganization of collagen, nuclear rounding, and angiogenesis) than the control and IL1-RA group. No significant difference in mechanical properties of the tendon was noted. These findings demonstrate IL1-RA can reduce pathologic changes in the patellar tendon in an established tendonitis model although did not demonstrate a difference in mechanical properties.

摘要

白细胞介素-1 (IL1) 是一种细胞因子,在炎症中发挥作用,是肌腱病中炎症的潜在贡献者。其抑制可能对肌腱病的治疗有用,并且一直是治疗的目标。为了评估白细胞介素 1 受体拮抗剂 (IL1-RA) 如何逆转与已建立的髌腱病相关的病理变化,我们将 48 只斯普拉格-道利退休种鼠随机分为三组,每周双侧髌腱注射 6 周。对照组接受 6 周 0.1ml 生理盐水。干预组用 0.1ml 2%卡拉胶治疗 4 周。从第 3 周开始,IL1-RA 组在最后 2 周内将 0.1ml 2%卡拉胶中添加 0.94mgIL1-RA(2.5mg/kg)和单独添加 0.94mgIL1-RA,而 CAR 组在最后 2 周内接受 0.1ml 生理盐水。初次注射后 6 周处死动物。CAR 组的肌腱长度明显(P<0.05)比对照组(7.81±0.44mm)和 IL1-RA 组(8.34±0.52mm)短(7.81±0.44mm)(P<0.05)。大体上,与 CAR 组相比,IL1-RA 组斑块样形成减少,肌腱边缘更明显。CAR 组的组织病理学变化(炎症细胞密度、胶原排列紊乱、核圆化和血管生成)明显大于对照组和 IL1-RA 组。肌腱力学性能无显著差异。这些发现表明,IL1-RA 可以减少已建立的肌腱炎模型中髌腱的病理变化,尽管在机械性能方面没有差异。